The Project Gutenberg eBook of Bodily changes in pain, hunger, fear, and rage
This ebook is for the use of anyone anywhere in the United States and
most other parts of the world at no cost and with almost no restrictions
whatsoever. You may copy it, give it away or re-use it under the terms
of the Project Gutenberg License included with this ebook or online
at www.gutenberg.org. If you are not located in the United States,
you will have to check the laws of the country where you are located
before using this eBook.
Title: Bodily changes in pain, hunger, fear, and rage
Author: Walter Bradford Cannon
Release date: June 28, 2024 [eBook #73932]
Language: English
Original publication: New York: D. Appleton and Company, 1915
Credits: Peter Becker, Neil Mercer and the Online Distributed Proofreading Team at https://www.pgdp.net (This file was produced from images generously made available by The Internet Archive)
*** START OF THE PROJECT GUTENBERG EBOOK BODILY CHANGES IN PAIN, HUNGER, FEAR, AND RAGE ***
Transcriber's Note
The List of Illustrations following the "Contents" section has been
added by the transcriber; the wording of captions in that List has
in some cases been condensed from the captions in the body of the
book.
Italic font is indicated by _underscores_.
BODILY CHANGES
IN PAIN, HUNGER,
FEAR AND RAGE
BODILY CHANGES
IN PAIN, HUNGER,
FEAR AND RAGE
AN ACCOUNT OF RECENT RESEARCHES
INTO THE FUNCTION
OF EMOTIONAL EXCITEMENT
BY
WALTER B. CANNON
GEORGE HIGGINSON PROFESSOR OF PHYSIOLOGY IN
HARVARD UNIVERSITY
[Illustration]
NEW YORK AND LONDON
D. APPLETON AND COMPANY
1915
Copyright, 1915, by
D. APPLETON AND COMPANY
Printed in the United States of America
TO MY COLLABORATORS IN THESE RESEARCHES
DANIEL DE LA PAZ
ALFRED T. SHOHL
WADE S. WRIGHT
ARTHUR L. WASHBURN
HENRY LYMAN
LEONARD B. NICE
CHARLES M. GRUBER
HOWARD OSGOOD
HORACE GRAY
WALTER L. MENDENHALL
WITH PLEASANT MEMORIES OF OUR
WORK TOGETHER
PREFACE
Fear, rage and pain, and the pangs of hunger are all primitive
experiences which human beings share with the lower animals.
These experiences are properly classed as among the most powerful
that determine the action of men and beasts. A knowledge of the
conditions which attend these experiences, therefore, is of general
and fundamental importance in the interpretation of behavior.
During the past four years there has been conducted, in the Harvard
Physiological Laboratory, a series of investigations concerned with
the bodily changes which occur in conjunction with pain, hunger
and the major emotions. A group of remarkable alterations in the
bodily economy have been discovered, all of which can reasonably be
regarded as responses that are nicely adapted to the individual’s
welfare and preservation. Because these physiological adaptations
are interesting both in themselves and in their interpretation,
not only to physiologists and psychologists, but to others as
well, it has seemed worth while to gather together in convenient
form the original accounts of the experiments, which have been
published in various American medical and physiological journals.
I have, however, attempted to arrange the results and discussions
in an orderly and consecutive manner, and I have tried also to
eliminate or incidentally to explain the technical terms, so that
the exposition will be easily understood by any intelligent reader
even though not trained in the medical sciences.
My first interest in the conditions attending pain, hunger and strong
emotional states was stimulated during the course of a previous
series of researches on the motor activities of the alimentary
canal. A summary of these researches appeared in 1911, under the
title, “The Mechanical Factors of Digestion.” The studies recorded
in the present volume may be regarded as a natural sequence of
observations on the influence of emotional states on the digestive
process, which were reported in that volume.
W. B. Cannon.
CONTENTS
CHAPTER I
PAGES
THE EFFECT OF THE EMOTIONS ON DIGESTION
Emotions favorable to normal secretion of the digestive
juices--Emotions unfavorable to normal secretion of
the digestive juices--Emotions favorable and unfavorable
to contractions of the stomach and intestines--The
disturbing effect of pain on digestion 1-21
CHAPTER II
THE GENERAL ORGANIZATION OF THE VISCERAL
NERVES CONCERNED IN EMOTIONS
The outlying neurones--The three divisions of the outlying
neurones--The extensive distribution of neurones
of the “sympathetic” or thoracico-lumbar division
and their arrangement for diffuse action--The
arrangement of neurones of the cranial and sacral
divisions for specific action--The cranial division a
conserver of bodily resources--The sacral division
a group of mechanisms for emptying--The sympathetic
division antagonistic to both the cranial and
the sacral--Neurones of the sympathetic division and
adrenal secretion have the same action 22-39
CHAPTER III
METHODS OF DEMONSTRATING ADRENAL SECRETION
AND ITS NERVOUS CONTROL
The evidence that splanchnic stimulation induces adrenal
secretion--The question of adrenal secretion
in emotional excitement--The method of securing
blood from near the adrenal veins--The method of
testing the blood for adrenin 40-51
CHAPTER IV
ADRENAL SECRETION IN STRONG EMOTIONS
AND PAIN
The evidence that adrenal secretion is increased in emotional
excitement--The evidence that adrenal secretion
is increased by “painful” stimulation--Confirmation
of our results by other observers 52-65
CHAPTER V
THE INCREASE OF BLOOD SUGAR IN PAIN AND
GREAT EMOTION
Glycosuria from pain--Emotional glycosuria--The rôle
of the adrenal glands in emotional glycosuria 66-80
CHAPTER VI
IMPROVED CONTRACTION OF FATIGUED MUSCLE
AFTER SPLANCHNIC STIMULATION OF THE
ADRENAL GLAND
The nerve-muscle preparation--The splanchnic preparation--The
effects of splanchnic stimulation on the
contraction of fatigued muscle--The first rise in the
muscle record--The prolonged rise in the muscle
record--The two factors: arterial pressure and adrenal
secretion 81-94
CHAPTER VII
THE EFFECTS ON CONTRACTION OF FATIGUED
MUSCLE OF VARYING THE ARTERIAL
BLOOD PRESSURE
The effect of increasing arterial pressure--The effect of
decreasing arterial pressure--An explanation of the
effects of varying the arterial pressure--The value
of increased arterial pressure in pain and strong
emotion 95-109
CHAPTER VIII
THE SPECIFIC RÔLE OF ADRENIN IN COUNTERACTING
THE EFFECTS OF FATIGUE
Variations of the threshold stimulus as a measure of
irritability--The method of determining the threshold
stimulus--The lessening of neuro-muscular irritability
by fatigue--The slow restoration of fatigued
muscle to normal irritability by rest--The quick restoration
of fatigued muscle to normal irritability
by adrenin--The evidence that the restorative action
of adrenin is specific--The point of action of
adrenin in muscle 110-134
CHAPTER IX
THE HASTENING OF THE COAGULATION OF BLOOD
BY ADRENIN
The graphic method of measuring the coagulation time--The
effects of subcutaneous injections of adrenin--The
effects of intravenous injections--The hastening
of coagulation by adrenin not a direct effect on the
blood 135-160
CHAPTER X
THE HASTENING OF COAGULATION OF BLOOD IN
PAIN AND GREAT EMOTION
Coagulation hastened by splanchnic stimulation--Coagulation
not hastened by splanchnic stimulation if
the adrenal glands are absent--Coagulation hastened
by “painful” stimulation--Coagulation hastened
in emotional excitement 161-183
CHAPTER XI
THE UTILITY OF THE BODILY CHANGES IN PAIN
AND GREAT EMOTION
The reflex nature of bodily responses in pain and the
major emotions, and the useful character of reflexes--The
utility of the increased blood sugar as
a source of muscular energy--The utility of increased
adrenin in the blood as an antidote to the
effects of fatigue--The question whether adrenin
normally secreted inhibits the use of sugar in the
body--The vascular changes produced by adrenin
favorable to supreme muscular exertion--The changes
in respiratory function also favorable to great effort--The
effects produced in asphyxia similar to those
produced in pain and excitement--The utility of
rapid coagulation in preventing loss of blood 184-214
CHAPTER XII
THE ENERGIZING INFLUENCE OF EMOTIONAL EXCITEMENT
“Reservoirs of power”--The excitements and energies of
competitive sports--Frenzy and endurance in ceremonial
and other dances--The fierce emotions and
struggles of battle--The stimulating influence of
witnesses and of music--The feeling of power 215-231
CHAPTER XIII
THE NATURE OF HUNGER
Appetite and hunger--The sensation of hunger--The
theory that hunger is a general sensation--Weakness
of the assumptions underlying the theory that
hunger is a general sensation--Body need may exist
without hunger--The theory that hunger is of general
origin does not explain the quick onset and the
periodicity of the sensation--The theory that hunger
is of general origin does not explain the local reference--Hunger
not due to emptiness of the stomach--Hunger
not due to hydrochloric acid in the empty
stomach--Hunger not due to turgescence of the gastric
mucous membrane--Hunger the result of contractions--The
“empty” stomach and intestines contract--Observations
suggesting that contractions
cause hunger--The concomitance of contractions and
hunger in man 232-266
CHAPTER XIV
THE INTERRELATIONS OF EMOTIONS
Antagonism between emotions expressed in the sympathetic
and in the cranial divisions of the autonomic
system--Antagonism between emotions expressed
in the sympathetic and in the sacral divisions
of the autonomic system--The function of
hunger--The similarity of visceral effects in different
strong emotions and suggestions as to its psychological
significance 267-284
CHAPTER XV
ALTERNATIVE SATISFACTIONS FOR THE FIGHTING
EMOTIONS
Support for the militarist estimate of the strength of
the fighting emotions and instincts--Growing opposition
to the fighting emotions and instincts as
displayed in war--The desirability of preserving the
martial virtues--Moral substitutes for warfare--Physical
substitutes for warfare--The significance of international
athletic competitions 285-301
A LIST OF PUBLISHED RESEARCHES FROM THE
PHYSIOLOGICAL LABORATORY IN HARVARD
UNIVERSITY 302-303
INDEX 305
LIST OF ILLUSTRATIONS
Figure Page
1. Diagram of the more important distributions of the
autonomic nervous system 25
2. Diagram of the arrangements for recording contractions of
the intestinal muscle 49
3. Intestinal muscle beating in inactive blood 53
4. Alternate application of “excited” blood and “quiet”
blood, from the same animal, to intestinal muscle initially
beating in Ringer’s solution 55
5. The effect of prolonging the excitement 55
6. Failure of the cava blood to produce inhibition when
excitement has occurred after removal of the adrenal glands 57
7. Effect of adding adrenin to formerly inactive blood 58
8. The effect of bubbling oxygen through active blood 59
9. Intestinal muscle beating in normal vena cava blood 62
10. The shielded electrodes used in stimulating the splanchnic
nerves 87
11. Contraction of the _tibialis anticus_ and stimulation
of the left splanchnic nerves 89
12. Arterial blood pressure with membrane manometer,
contractions of _tibialis anticus_, and splanchnic
stimulation 91
13-17. Effect of varying arterial blood pressure upon muscular
contraction over time 98-104
18. Threshold stimulus of muscles during an experiment 116
19. Threshold stimulus of muscles during an experiment 122
20. Threshold stimulus of muscles during an experiment 124
21. Effect of adrenin injection upon blood pressure and
contractions of the _tibialis anticus_ muscle 128
22. Effect of amyl nitrite injection upon blood pressure and
contractions of the _tibialis anticus_ muscle 128
23. Effect of adrenin injection upon blood pressure and
contractions of the _tibialis anticus_ muscle
when denervated 131
24. Diagram of the graphic coagulometer 139
25. Record of five successive tests of coagulation 145
26. Shortening of coagulation time after injection of adrenin 151
27. Differing effects upon the coagulation time of slow and
rapid injections of adrenin 153
28. Persistent shortening of the coagulation time after
injection of adrenin when brain and upper cord pithed 154
29. Shortening of coagulation time after stimulation of
the left splanchnic nerves 163
30. Shortening of coagulation time after stimulation of
the left splanchnic nerves 164
31. Results of stimulating the left splanchnic nerves after
removal of the left adrenal gland; and of stimulating
the right splanchnic nerves with right adrenal gland
present 169
32. Three shortenings of coagulation time after stimulation
of the left sciatic nerve 174
33. Shortening of coagulation time during an operation
under light anesthesia 175
34. Record of rapid clotting after emotional excitement 180
35. Rapid clotting after emotional excitement, with slowing
of the process when the splanchnic nerves were cut in the
thorax 182
36. Adrenal secretion produced by asphyxia 208
37. Intragastric pressure, respiration and report of
hunger pangs against time 257
38. The same conditions as in Fig. 37 259
39. Compression of thin rubber bag in the lower esophagus,
and report of hunger pangs against time 260
BODILY CHANGES IN PAIN, HUNGER, FEAR AND RAGE
CHAPTER I
THE EFFECT OF THE EMOTIONS ON DIGESTION
The doctrine of human development from subhuman antecedents has
done much to unravel the complex nature of man. As a means of
interpretation this doctrine has been directed chiefly toward the
solving of puzzles in the peculiarities of anatomical structure. Thus
arrangements in the human body, which are without obvious utility,
receive rational explanation as being vestiges of parts useful in or
characteristic of remote ancestors--parts retained in man because
of age-long racial inheritance. This mode of interpretation has
proved applicable also in accounting for functional peculiarities.
Expressive actions and gestures--the facial appearance in anger,
for example--observed in children and in widely distinct races,
are found to be innate, and are best explained as the retention in
human beings of responses which are similar in character in lower
animals.
From this point of view biology has contributed much to clarify
our ideas regarding the motives of human behavior. The social
philosophies which prevailed during the past century either assumed
that conduct was determined by a calculated search for pleasure
and avoidance of pain or they ascribed it to a vague and undefined
faculty named the conscience or the moral sense. Comparative study of
the behavior of men and of lower animals under various circumstances,
however, especially with the purpose of learning the source of
prevailing impulses, is revealing the inadequacy of the theories
of the older psychologists. More and more it is appearing that in
men of all races and in most of the higher animals, the springs of
action are to be found in the influence of certain emotions which
express themselves in characteristic instinctive acts.
The rôle which these fundamental responses in the higher organisms
play in the bodily economy has received little attention. As a realm
for investigation the bodily changes in emotional excitement have
been left by the physiologists to the philosophers and psychologists
and to the students of natural history. These students, however,
have usually had too slight experience in the detailed examination
of bodily functions to permit them to follow the clues which
superficial observation might present. In consequence our knowledge
of emotional states has been meager.
There are, of course, many surface manifestations of excitement. The
contraction of blood vessels with resulting pallor, the pouring out
of “cold sweat,” the stopping of saliva-flow so that the “tongue
cleaves to the roof of the mouth,” the dilation of the pupils, the
rising of the hairs, the rapid beating of the heart, the hurried
respiration, the trembling and twitching of the muscles, especially
those about the lips--all these bodily changes are well recognized
accompaniments of pain and great emotional disturbance, such as
fear, horror and deep disgust. But these disturbances of the
even routine of life, which have been commonly noted, are mainly
superficial and therefore readily observable. Even the increased
rapidity of the heart beat is noted at the surface in the pulsing
of the arteries. There are, however, other organs, hidden deep in
the body, which do not reveal so obviously as the structures near
or in the skin, the disturbances of action which attend states of
intense feeling. Special methods must be used to determine whether
these deep-lying organs also are included in the complex of an
emotional[*] agitation.
*[Footnote: In the use of the term “emotion” the meaning here is
not restricted to violent affective states, but includes “feelings”
and other affective experiences. At times, also, in order to avoid
awkward expressions, the term is used in the popular manner, as
if the “feeling” caused the bodily change.]
Among the organs that are affected to an important degree by
feelings are those concerned with digestion. And the relations of
feelings to the activities of the alimentary canal are of particular
interest, because recent investigations have shown that not only
are the first stages of the digestive process normally started by
the pleasurable taste and smell and sight of food, but also that
pain and great emotional excitement can seriously interfere with
the starting of the process or its continuation after it has been
started. Thus there may be a conflict of feelings and of their
bodily accompaniments--a conflict the interesting bearing of which
we shall consider later.
Emotions Favorable to Normal Secretion of the
Digestive Juices
The feelings or affective states favorable to the digestive functions
have been studied fruitfully by Pawlow,[1] of Petrograd, through
ingenious experiments on dogs. By the use of careful surgical methods
he was able to make a side pouch of a part of the stomach, the
cavity of which was wholly separate from the main cavity in which
the food was received. This pouch was supplied in a normal manner
with nerves and blood vessels, and as it opened to the surface of
the body, the amount and character of the gastric juice secreted
by it under various conditions could be accurately determined.
Secretion by that part of the stomach wall which was included in the
pouch was representative of the secretory activities of the entire
stomach. The arrangement was particularly advantageous in providing
the gastric juice unmixed with food. In some of the animals thus
operated upon an opening was also made in the esophagus so that when
the food was swallowed, it did not pass to the stomach but dropped
out on the way. All the pleasures of eating were thus experienced,
and there was no necessity of stopping because of a sense of fulness.
This process was called “sham feeding.” The well-being of these
animals was carefully attended to, they lived the normal life of
dogs, and in the course of months and years became the pets of the
laboratory.
By means of sham feeding Pawlow showed that the chewing and
swallowing of food which the dogs relished resulted, after a delay
of about five minutes, in a flow of natural gastric juice from the
side pouch of the stomach--a flow which persisted as long as the dog
chewed and swallowed the food, and continued for some time after
eating ceased. Evidently the presence of food in the stomach is not
a prime condition for gastric secretion. And since the flow occurred
only when the dogs had an appetite, and the material presented to
them was agreeable, the conclusion was justified that this was a
true psychic secretion.
The mere sight or smell of a favorite food may start the pouring
out of gastric juice, as was noted many years ago by Bidder and
Schmidt[2] in a hungry dog which had a fistulous opening through the
body wall into the stomach. This observation, reported in 1852, was
confirmed later by Schiff and also still later by Pawlow. That the
mouth “waters” with a flow of saliva when palatable food is seen or
smelled has long been such common knowledge that the expression,
“It makes my mouth water,” is at once recognized as the highest
testimony to the attractiveness of an appetizing dish. That the
stomach also “waters” in preparation for digesting the food which
is to be taken is clearly proved by the above cited observations
on the dog.
The importance of the initial psychic secretion of saliva for
further digestion is indicated when, in estimating the function
of taste for the pleasures of appetite, we realize that materials
can be tasted only when dissolved in the mouth and thereby brought
into relation with the taste organs. The saliva which “waters” the
mouth assures the dissolving of dry but soluble food even when it
is taken in large amount.
The importance of the initial psychic secretion of gastric juice
is made clear by the fact that continuance of the flow of this
juice during digestion is provided by the action of its acid or its
digestive products on the mucous membrane of the pyloric end of the
stomach, and that secretion of the pancreatic juice and bile are
called forth by the action of this same acid on the mucous membrane
of the duodenum. The proper starting of the digestive process,
therefore, is conditioned by the satisfactions of the palate, and
the consequent flow of the first digestive fluids.
The facts brought out experimentally in studies on lower animals
are doubtless true also of man. Not very infrequently, because of
the accidental swallowing of corrosive substances, the esophagus
is so injured that, when it heals, the sides grow together and the
tube is closed. Under these circumstances an opening has to be
made into the stomach through the side of the body and then the
individual chews his food in the usual manner, but ejects it from
his mouth into a tube which is passed through the gastric opening.
The food thus goes from mouth to stomach through a tube outside the
chest instead of inside the chest. As long ago as 1878, Richet,[3]
who had occasion to study a girl whose esophagus was closed and
who was fed through a gastric fistula, reported that whenever the
girl chewed or tasted a highly sapid substance, such as sugar or
lemon juice, while the stomach was empty, there flowed from the
fistula a considerable quantity of gastric juice. A number of later
observers[4] have had similar cases in human beings, especially
in children, and have reported in detail results which correspond
remarkably with those obtained in the laboratory. Hornborg[4] found
that when the little boy whom he studied chewed agreeable food a
more or less active secretion of gastric juice invariably started,
whereas the chewing of an indifferent substance, as gutta-percha, was
followed by no secretion. All these observations clearly demonstrate
that the normal flow of the first digestive fluids, the saliva and
the gastric juice, is favored by the pleasurable feelings which
accompany the taste and smell of food during mastication, or which
are roused in anticipation of eating when choice morsels are seen
or smelled.
These facts are of fundamental importance in the serving of food,
especially when, through illness, the appetite is fickle. The
degree of daintiness with which nourishment is served, the little
attentions to esthetic details--the arrangement of the dishes, the
small portions of food, the flower beside the plate--all may help
to render food pleasing to the eye and savory to the nostrils and
may be the deciding factors in determining whether the restoration
of strength is to begin or not.
Emotions Unfavorable to the Normal Secretion of the
Digestive Juices
The conditions favorable to proper digestion are wholly abolished
when unpleasant feelings such as vexation and worry and anxiety,
or great emotions such as anger and fear, are allowed to prevail.
This fact, so far as the salivary secretion is concerned, has long
been known. The dry mouth of the anxious person called upon to
speak in public is a common instance; and the “ordeal of rice,” as
employed in India, was a practical utilization of the knowledge
that excitement is capable of inhibiting the salivary flow. When
several persons were suspected of crime, the consecrated rice was
given to them all to chew, and after a short time it was spit out
upon the leaf of the sacred fig tree. If anyone ejected it dry,
that was taken as proof that fear of being discovered had stopped
the secretion, and consequently he was adjudged guilty.[5]
What has long been recognized as true of the secretion of saliva
has been proved true also of the secretion of gastric juice. For
example, Hornborg was unable to confirm in his little patient with
a gastric fistula the observation by Pawlow that when hunger is
present the mere seeing of food results in a flow of gastric juice.
Hornborg explained the difference between his and Pawlow’s results
by the different ways in which the boy and the dogs faced the
situation. When food was shown, but withheld, the hungry dogs were
all eagerness to secure it, and the juice very soon began to flow.
The boy, on the contrary, became vexed when he could not eat at
once, and began to cry; then no secretion appeared. Bogen also has
reported the instance of a child with closed esophagus and gastric
fistula, who sometimes fell into such a passion in consequence of
vain hoping for food that the giving of the food, after the child
was calmed, was not followed by any flow of the secretion.
The inhibitory influence of excitement has also been seen in lower
animals under laboratory conditions. Le Conte[6] declares that in
studying gastric secretion it is necessary to avoid all circumstances
likely to provoke emotional reactions. In the fear which dogs
manifest when first brought into strange surroundings he found
that activity of the gastric glands may be completely suppressed.
The suppression occurred even if the dog had eaten freely and was
then disturbed--as, for example, by being tied to a table. When
the animals became accustomed to the experimental procedure, it no
longer had an inhibitory effect. The studies of Bickel and Sasaki[7]
confirm and define more precisely this inhibitory effect of strong
emotion on gastric secretion. They observed the inhibition on a dog
with an esophageal fistula, and with a side pouch of the stomach,
which, as in Pawlow’s experiments, opened only to the exterior. In
this dog Bickel and Sasaki noted, as Pawlow had, that sham feeding
was attended by a copious flow of gastric juice, a true psychic
secretion, resulting from the pleasurable taste of the food. In
a typical instance the sham feeding lasted five minutes, and the
secretion continued for twenty minutes, during which time 66.7
cubic centimeters of pure gastric juice were produced.
On another day a cat was brought into the presence of the dog,
whereupon the dog flew into a great fury. The cat was soon removed,
and the dog pacified. Now the dog was again given the sham feeding
for five minutes. In spite of the fact that the animal was hungry
and ate eagerly, there was no secretion worthy of mention. During a
period of twenty minutes, corresponding to the previous observation,
only 9 cubic centimeters of acid fluid were produced, and this
was rich in mucus. It is evident that in the dog, as in the boy
observed by Bogen, strong emotions can so profoundly disarrange
the mechanisms of secretion that the pleasurable excitation which
accompanies the taking of food cannot cause the normal flow.
On another occasion Bickel and Sasaki started gastric secretion in
the dog by sham feeding, and when the flow of gastric juice had
reached a certain height, the dog was infuriated for five minutes
by the presence of the cat. During the next fifteen minutes there
appeared only a few drops of a very mucous secretion. Evidently in
this instance a physiological process, started as an accompaniment
of a psychic state quietly pleasurable in character, was almost
entirely stopped after another psychic state violent in character.
It is noteworthy that in both the favorable and unfavorable results
of the emotional excitement illustrated in Bickel and Sasaki’s
dog the effects persisted long after the removal of the exciting
condition. This fact, in its favorable aspect, Bickel[8] was able
to confirm in a girl with esophageal and gastric fistulas; the
gastric secretion long outlasted the period of eating, although no
food entered the stomach. The influences unfavorable to digestion,
however, are stronger than those which promote it. And evidently,
if the digestive process, because of emotional disturbance, is
for some time inhibited, the swallowing of food which must lie
stagnant in the stomach is a most irrational procedure. If a child
has experienced an outburst of passion, it is well not to urge the
taking of nourishment soon afterwards. Macbeth’s advice that “good
digestion wait on appetite and health on both,” is now well-founded
physiology.
Other digestive glands than the salivary and the gastric may be
checked in emotional excitement. Recently Oechsler[9] has reported
that in such psychic disturbances as were shown by Bickel and Sasaki
to be accompanied by suppressed secretion of the gastric juice,
the secretion of pancreatic juice may be stopped, and the flow of
bile definitely checked. All the means of bringing about chemical
changes in the food may be thus temporarily abolished.
Emotions Favorable and Unfavorable to the Contractions
of the Stomach and Intestines
The secretions of the digestive glands and the chemical changes
wrought by them are of little worth unless the food is carried
onward through the alimentary canal into fresh regions of digestion
and is thoroughly exposed to the intestinal wall for absorption.
In studying these mechanical aspects of digestion I was led to
infer[10] that just as there is a psychic secretion, so likewise
there is probably a “psychic tone” or “psychic contraction” of
the gastro-intestinal muscles as a result of taking food. For if
the vagus nerve supply to the stomach is cut immediately _before_
an animal takes food, the usual contractions of the gastric wall,
as seen by the Röntgen rays, do not occur; but if these nerves
are cut _after_ food has been eaten with relish, the contractions
which have started continue without cessation. The nerves in both
conditions were severed under anesthesia, so that no element of
pain entered into the experiments. In the absence of hunger, which
in itself provides a contracted stomach,[11] the pleasurable taking
of food may, therefore, be a primary condition for the appearance
of natural contractions of the gastro-intestinal canal.
Again just as the secretory activities of the stomach are unfavorably
influenced by strong emotions, so also are the movements of the
stomach; and, indeed, the movements of almost the entire alimentary
canal are wholly stopped during great excitement. In my earliest
observations on the movements of the stomach[12] I had difficulty
because in some animals the waves of contraction were perfectly
evident, while in others there was no sign of activity. Several
weeks passed before I discovered that this difference was associated
with a difference of sex. In order to be observed with Röntgen
rays the animals were restrained in a holder. Although the holder
was comfortable, the male cats, particularly the young males,
were restive and excited on being fastened to it, and under these
circumstances gastric peristaltic waves were absent; the female
cats, especially if elderly, usually submitted with calmness to the
restraint, and in them the waves had their normal occurrence. Once
a female with kittens turned from her state of quiet contentment
to one of apparent restless anxiety. The movements of the stomach
immediately stopped, the gastric wall became wholly relaxed, and
only after the animal had been petted and began to purr did the
moving waves start again on their course. By covering the cat’s mouth
and nose with the fingers until a slight distress of breathing is
produced, the stomach contractions can be stopped at will. In the
cat, therefore, any sign of rage or fear, such as was seen in dogs
by Le Conte and by Bickel and Sasaki, was accompanied by a total
abolition of the movements of the stomach. Even indications of slight
anxiety may be attended by complete absence of the churning waves.
In a vigorous young male cat I have watched the stomach for more
than an hour by means of the Röntgen rays, and during that time not
the slightest beginning of peristaltic activity appeared; yet the
only visible indication of excitement in the animal was a continued
quick twitching of the tail to and fro. What is true of the cat I
have found true also of the rabbit, dog and guinea-pig[13]--very mild
emotional disturbances are attended by abolition of peristalsis.
The observations on the rabbit have been confirmed by Auer,[14]
who found that the handling of the animal incidental to fastening
it gently to a holder stopped gastric peristalsis for a variable
length of time. And if the animal was startled for any reason,
or struggled excitedly, peristalsis was again abolished. The
observations on the dog also have been confirmed; Lommel[15] found
that small dogs in strange surroundings might have no contractions
of the stomach for two or three hours. And whenever the animals
showed any indications of being uncomfortable or distressed, the
contractions were inhibited and the discharge of contents from the
stomach checked.
Like the peristaltic waves in the stomach, the peristalsis and the
kneading movements (segmentation) in the small intestine, and the
reversed peristalsis in the large intestine all cease whenever the
observed animal shows signs of emotional excitement.
There is no doubt that just as the secretory activity of the stomach
is affected in a similar fashion in man and in lower animals, so
likewise gastric and intestinal peristaltic waves are stopped in
man as they are stopped in lower animals, by worry and anxiety and
the stronger affective states. The conditions of mental discord
may thus give rise to a sense of gastric inertia. For example, a
patient described by Müller[16] testified that anxiety was always
accompanied by a feeling of weight, as if the food remained in
the stomach. Every addition of food caused an increase of the
trouble. Strong emotional states in this instance led almost always
to gastric distress, which persisted, according to the grade and
the duration of the psychic disturbance, between a half-hour and
several days. The patient was not hysterical or neurasthenic, but
was a very sensitive woman deeply affected by moods.
The feeling of heaviness in the stomach, mentioned in the foregoing
case, is not uncommonly complained of by nervous persons, and may be
due to stagnation of the contents. That such stagnation occurs is
shown by the following instance. A refined and sensitive woman, who
had had digestive difficulties, came with her husband to Boston to
be examined. They went to a hotel for the night. The next morning
the woman appeared at the consultant’s office an hour after having
eaten a test meal. An examination of the gastric contents revealed
no free acid, no digestion of the test breakfast, and the presence
of a considerable amount of the supper of the previous evening.
The explanation of this stagnation of the food in the stomach came
from the family doctor, who reported that the husband had made the
visit to the city an occasion for becoming uncontrollably drunk, and
that he had by his escapades given his wife a night of turbulent
anxiety. The second morning, after the woman had had a good rest,
the gastric contents were again examined; the proper acidity
was found, and the test breakfast had been normally digested and
discharged.
These cases are merely illustrative and doubtless can be many times
duplicated in the experience of any physician concerned largely with
digestive disorders. Indeed, the opinion has been expressed that a
great majority of the cases of gastric indigestion that come for
treatment are functional in character and of nervous origin. It is
the emotional element that seems most characteristic of these cases.
To so great an extent is this true that Rosenbach has suggested that
as a term to characterize the cause of the disturbances, “emotional”
dyspepsia is better than “nervous” dyspepsia.[17]
The Disturbing Effect of Pain on Digestion
The advocates of the theory of organic evolution early pointed out
the similarity between the bodily disturbances in pain and in the
major emotions. The alterations of function of internal organs they
could not know about. The general statement, however, that pain
evokes the same changes that are evoked by emotion, is true also of
these deep-lying structures. Wertheimer[18] proved many years since
that stimulation of a sensory nerve in an anesthetized animal--such
stimulation as in a conscious animal would induce pain--quickly
abolished the contractions of the stomach. And Netschaiev, working
in Pawlow’s[19] laboratory, showed that excitation of the sensory
fibres in the sciatic nerve for two or three minutes resulted in
an inhibition of the secretion of gastric juice that lasted for
several hours. Similar effects from painful experience have been not
uncommonly noted in human beings. Mantegazza,[20] in his account of
the physiology of pain, has cited a number of such examples, and
from them he has concluded that pain interferes with digestion by
lessening appetite and by producing various forms of dyspepsia, with
arrest of gastric digestion, and with vomiting and diarrhea. The
expression, “sickening pain” is testimony to the power of strong
sensory stimulation to upset the digestive processes profoundly.
Vomiting is as likely to follow violent pain as it is to follow
strong emotion. A “sick headache” may be, indeed, a sequence of
events in which the pain from the headache is primary, and the
nausea and other evidences of digestive disorder are secondary.
As the foregoing account has shown, emotional conditions or
“feelings” may be accompanied by quite opposite effects in the
alimentary canal, some highly favorable to good digestion, some
highly disturbing. It is an interesting fact that the feelings having
these antagonistic actions are typically expressed through nerve
supplies which are correspondingly opposed in their influence on the
digestive organs. The antagonism between these nerve supplies is
of fundamental importance in understanding not only the operation
of conditions favorable or unfavorable to digestion but also in
obtaining insight into the conflicts of emotional states. Since a
consideration of the arrangement and mode of action of these nerves
will establish a firm basis for later analysis and conclusions,
they will next be considered.
REFERENCES
[Footnote 1: Pawlow: The Work of the Digestive Glands, London,
1902.]
[Footnote 2: Bidder and Schmidt: Die Verdauungssäfte und der
Stoffwechsel, Leipzig, 1852, p. 35.]
[Footnote 3: Richet: Journal de l’Anatomie et de la Physiologie,
1878, xiv, p. 170.]
[Footnote 4: See Hornborg: Skandinavisches Archiv für Physiologie,
1904, xv, p. 248. Cade and Latarjet: Journal de Physiologie et
Pathologie Générale, 1905, vii, p. 221. Bogen: Archiv für die
gesammte Physiologie, 1907, cxvii, p. 156. Lavenson: Archives of
Internal Medicine, 1909, iv, p. 271.]
[Footnote 5: Lea: Superstition and Force, Philadelphia, 1892, p.
344.]
[Footnote 6: Le Conte: La Cellule, 1900, xvii, p. 291.]
[Footnote 7: Bickel and Sasaki: Deutsche medizinische Wochenschrift,
1905, xxxi, p. 1829.]
[Footnote 8: Bickel: Berliner klinische Wochenschrift, 1906, xliii,
p. 845.]
[Footnote 9: Oechsler: Internationelle Beiträge zur Pathologie und
Therapie der Ernährungstörungen, 1914, v, p. 1.]
[Footnote 10: Cannon: The Mechanical Factors of Digestion, London
and New York, 1911, p. 200.]
[Footnote 11: Cannon and Washburn: American Journal of Physiology,
1912, xxix, p. 441.]
[Footnote 12: Cannon: The American Journal of Physiology, 1898, i,
p. 38.]
[Footnote 13: Cannon: American Journal of Physiology, 1902, vii,
p. xxii.]
[Footnote 14: Auer: American Journal of Physiology, 1907, xviii,
p. 356.]
[Footnote 15: Lommel: Münchener medizinische Wochenschrift, 1903,
i, p. 1634.]
[Footnote 16: Müller: Deutsches Archiv für klinische Medicin, 1907,
lxxxix, p. 434.]
[Footnote 17: Rosenbach: Berliner klinische Wochenschrift, 1897,
xxxiv, p. 71.]
[Footnote 18: Wertheimer: Archives de Physiologie, 1892, xxiv, p.
379.]
[Footnote 19: Pawlow: _Loc. cit._, p. 56.]
[Footnote 20: Mantegazza: Fisiologia del Dolore, Florence, 1880,
p. 123.]
CHAPTER II
THE GENERAL ORGANIZATION OF THE VISCERAL NERVES
CONCERNED IN EMOTIONS
The structures of the alimentary canal which are brought into
activity during the satisfactions of appetite or are checked in
their activity during pain and emotional excitement are either the
secreting digestive glands or the smooth muscle which surrounds
the canal. Both the gland cells and the smooth-muscle cells differ
from other cells which are subject to nervous influence--those of
striated, or skeletal, muscle--in not being directly under voluntary
control and in being slower in their response. The muscle connected
with the skeleton responds to stimulation within two or three
thousandths of a second; the delay with gland cells and with smooth
muscle is more likely to be measured in seconds than in fractions
of a second.
The Outlying Neurones
The skeletal muscles receive their nerve supply direct from the
central nervous system, i. e., the nerve fibres distributed to these
muscles are parts of neurones whose cell bodies lie within the brain
or spinal cord. The glands and smooth muscles of the viscera, on the
contrary, are, so far as is now known, never innervated directly
from the central nervous system.[*] The neurones reaching out from
the brain or spinal cord never come into immediate relation with the
gland or smooth-muscle cells; there are always interposed between the
cerebrospinal neurones and the viscera extra neurones whose bodies
and processes lie wholly outside the central nervous system. They
are represented in dotted lines in Fig. 1. I have suggested that
possibly these outlying neurones act as “transformers,” modifying the
impulses received from the central source (impulses suited to call
forth the quick responses of _skeletal_ muscle), and adapting these
impulses to the peculiar, more slowly-acting tissues, the secreting
cells and visceral muscle, to which they are distributed.[21]
*[Footnote: The special case of the adrenal glands will be
considered later.]
The outlying neurones typically have their cell bodies grouped in
ganglia (G’s, Fig. 1) which, in the trunk region, lie along either
side of the spinal cord and in the head region and in the pelvic
part of the abdominal cavity are disposed near the organs which the
neurones supply. In some instances these neurones lie wholly within
the structure which they innervate (see e. g., the heart and the
stomach, Fig. 1). In other instances the fibres passing out from
the ganglia--the so-called “postganglionic fibres”--may traverse
long distances before reaching their destination. The innervation
of blood vessels in the foot by neurones whose cell bodies are in
the lower trunk region is an example of this extensive distribution
of the fibres.
[Illustration: Figure 1.--Diagram of the more important
distributions of the autonomic nervous system. The brain and spinal
cord are represented at the left. The nerves to skeletal muscles
are not represented. The preganglionic fibres of the autonomic
system are in solid lines, the postganglionic in dash-lines. The
nerves of the cranial and sacral divisions are distinguished from
those of the thoracico-lumbar or “sympathetic” division by broader
lines. A + mark indicates an augmenting effect on the activity
of the organ; a - mark, a depressive or inhibitory effect. For
further description see text.]
The Three Divisions of the Outlying Neurones
As suggested above, the outlying neurones are connected with the
brain and spinal cord by neurones whose cell bodies lie within the
central nervous organs. These connecting neurones, represented in
continuous lines in Fig. 1, do not pass out in a continuous series
all along the cerebrospinal axis. Where the nerves pass out from
the spinal cord to the fore and hind limbs, fibres are not given
off to the ganglia. Thus these connecting or “preganglionic” fibres
are separated into three divisions. In front of the nerve roots
for the fore limbs is the head or cranial division, between the
nerve roots for the fore limbs and those for the hind limbs is the
trunk division (or thoracico-lumbar division, or, in the older
terminology, the “sympathetic system”); and after the nerve roots
for the hind limbs the sacral division.
This system of outlying neurones, with postganglionic fibres
innervating the viscera, and with preganglionic fibres reaching
out to them from the cerebrospinal system, has been called by
Langley, to whom we are indebted for most of our knowledge of its
organization, the _autonomic nervous system_.[22] This term indicates
that the structures which the system supplies are not subject to
voluntary control, but operate to a large degree independently. As
we have seen, a highly potent mode of influencing these structures
is through conditions of pain and emotional excitement. The parts
of the autonomic system--the cranial, the sympathetic, and the
sacral--have a number of peculiarities which are of prime importance
in accounting for the bodily manifestations of such affective states.
The Extensive Distribution of Neurones of the “Sympathetic”
Division and Their Arrangement for Diffuse Action
The fibres of the sympathetic division differ from those of the
other two divisions in being distributed through the body very
widely. They go to the eyes, causing dilation of the pupils. They go
to the heart and, when stimulated, they cause it to beat rapidly.
They carry impulses to arteries and arterioles of the skin, the
abdominal viscera, and other parts, keeping the smooth muscles
of the vessel walls in a state of slight contraction or tone,
and thus serving to maintain an arterial pressure sufficiently
high to meet sudden demands in any special region; or, in times
of special discharge of impulses, to increase the tone and thus
also the arterial pressure. They are distributed extensively to
the smooth muscle attached to the hairs; and when they cause this
muscle to contract, the hairs are erected. They go to sweat glands,
causing the outpouring of sweat. These fibres pass also to the
entire length of the gastro-intestinal canal. And the inhibition of
digestive activity which, as we have learned, occurs in pain and
emotional states, is due to impulses which are conducted outward
by the _splanchnic nerves_--the preganglionic fibres that reach to
the great ganglia in the upper abdomen (see Fig. 1)--and thence
are spread by postganglionic fibres all along the gut.[23] They
innervate likewise the genito-urinary tracts, causing contraction
of the smooth muscle of the internal genital organs, and usually
relaxation of the bladder. Finally they affect the liver, releasing
the storage of material there in a manner which may be of great
service to the body in time of need. The _extensiveness_ of the
distribution of the fibres of the sympathetic division is one of
its most prominent characteristics.
Another typical feature of the sympathetic division is an arrangement
of neurones for diffuse discharge of the nerve impulses. As shown
diagrammatically in Fig. 1, the preganglionic fibres from the
central nervous system may extend through several of the sympathetic
ganglia and give off in each of them connections to cell bodies of
the outlying neurones. Although the neurones which transmit sensory
impulses from the skin into spinal cord have similar relations to
nerve cells lying at different levels of the cord, the operation in
the two cases is quite different. In the spinal cord the sensory
impulse produces directed and closely limited effects, as, for
example, when reflexes are being evoked in a “spinal” animal (i. e.,
an animal with the spinal cord isolated from the rest of the central
nervous system), the left hind limb is nicely lifted, in response
to a harmful stimulus applied to the left foot, without widespread
marked involvement of the rest of the body in the response.[24]
In the action of the sympathetic division, on the contrary, the
connection of single preganglionic fibres with numerous outlying
neurones seems to be not at all arranged for specific effects in
this or that particular region. There are, to be sure, in different
circumstances variations in the degree of activity of different
parts; for example, it is probable that dilation of the pupil in the
cat occurs more readily than erection of the hairs. It may be in
this instance, however, that specially direct pathways to the eye
are present for common use in non-emotional states (in dim light,
e. g.), and that only slight general disturbance in the central
nervous system, therefore, would be necessary to send impulses
by these well-worn courses. Thus for local reasons (dust, e. g.)
tears might flow from excitation of the tear glands by sympathetic
impulses, although other parts innervated by this same division might
be but little disturbed. We have no means of voluntarily wearing
these pathways, however, and both from anatomical and physiological
evidence the neurone relations in the sympathetic division of the
autonomic system seem devised for widespread diffusion of nervous
impulses.
The Arrangement of Neurones of the Cranial and Sacral
Divisions for Specific Action
The cranial and sacral autonomic divisions differ from the
sympathetic in having only _restricted_ distribution (see Fig.
1). The third cranial nerves deliver impulses from the brain to
ganglia in which lie the cell bodies of neurones innervating
smooth muscle only in the front of the eyes. The vagus nerves are
distributed to the lungs, heart, stomach, and small intestine.
As shown diagrammatically in Fig. 1, the outlying neurones in
the last three of these organs lie within the organs themselves.
By this arrangement, although the preganglionic fibres of the
vagi are extended in various directions to structures of quite
diverse functions, singleness and separateness of connection of the
peripheral organs with the central nervous system is assured. The
same specific relation between efferent fibres and the viscera is
seen in the sacral autonomic. In this division the preganglionic
fibres pass out from the spinal cord to ganglia lying in close
proximity to the distal colon, the bladder, and the external
genitals. And the postganglionic fibres deliver the nerve impulses
only to the nearby organs. Besides these innervations the cranial
and sacral divisions supply individual arteries with “dilator
nerves”--nerves causing relaxation of the particular vessels. Quite
typically, therefore, the efferent fibres of the two terminal
divisions of the autonomic differ from those of the mid-division
in having few of the distributed connections characteristic of the
mid-division, and in innervating distinctively the organs to which
they are distributed. The cranial and sacral preganglionic fibres
resemble thus the nerves to skeletal muscles, and their arrangement
provides similar possibilities of specific and separate action in
any part, without action in other parts.
The Cranial Division a Conserver of Bodily Resources
The cranial autonomic, represented by the vagus nerves, is the part
of the visceral nervous system concerned in the psychic secretion
of the gastric juice. Pawlow showed that when these nerves are
severed psychic secretion is abolished. The cranial nerves to the
salivary glands are similarly the agents for psychic secretion in
these organs, and are known to cause also dilation of the arteries
supplying the glands, so that during activity the glands receive a
more abundant flow of blood. As previously stated (see p. 13), the
evidence for a psychic tonus of the gastro-intestinal musculature
rests on a failure of the normal contractions if the vagi are
severed before food is taken, in contrast to the continuance of the
contractions if the nerves are severed just afterwards. The vagi
artificially excited are well known as stimulators of increased
tone in the smooth muscle of the alimentary canal. Aside from these
positive effects on the muscles of the digestive tract and its
accessory glands, cranial autonomic fibres cause contraction of
the pupil of the eye, and slowing of the heart rate.
A glance at these various functions of the cranial division reveals
at once that they serve for bodily conservation. By narrowing the
pupil of the eye they shield the retina from excessive light. By
slowing the heart rate, they give the cardiac muscle longer periods
for rest and invigoration. And by providing for the flow of saliva
and gastric juice and by supplying the muscular tone necessary
for contraction of the alimentary canal, they prove fundamentally
essential to the processes of proper digestion and absorption by
which energy-yielding material is taken into the body and stored.
To the cranial division of the visceral nerves, therefore, belongs
the quiet service of building up reserves and fortifying the body
against times of need or stress.
The Sacral Division a Group of Mechanisms for Emptying
Sacral autonomic fibres cause contraction of the rectum and distal
colon and also contraction of the bladder. In both instances the
effects result reflexly from stretching of the tonically contracted
viscera by their accumulating contents. No affective states precede
this normal action of the sacral division and even those which
accompany or follow are only mildly positive; a feeling of relief
rather than of elation usually attends the completion of the act
of defecation or micturition--though there is testimony to the
contrary.
The sacral autonomic fibres also include, however, the nervi
erigentes which bring about engorgement of erectile tissue in the
external genitals. According to Langley and Anderson[25] the sacral
nerves have no effect on the _internal_ generative organs. The vasa
deferentia and the seminal vesicles whose rhythmic contractions
mark the acme of sexual excitement in the male, and the uterus whose
contractions in the female are probably analogous, are supplied
only by lumbar branches--part of the sympathetic division. These
branches also act in opposition to the nervi erigentes and cause
constriction of the blood vessels of the external genitals. The
sexual orgasm involves a high degree of emotional excitement; but
it can be rightly considered as essentially a reflex mechanism;
and, again in this instance, distention of tubules, vesicles, and
blood vessels can be found at the beginning of the incident, and
relief from this distention at the end.
Although distention is the commonest occasion for bringing the sacral
division into activity it is not the only occasion. Great emotion,
such as is accompanied by nervous discharges via the sympathetic
division, may also be accompanied by discharges via the sacral
fibres. The involuntary voiding of the bladder and lower gut at times
of violent mental stress is well known. Veterans of wars testify
that just before the beginning of a battle many of the men have to
retire temporarily from the firing line. And the power of sights and
smells and libidinous thoughts to disturb the regions controlled by
the nervi erigentes proves that this part of the autonomic system
also has its peculiar affective states. The fact that one part of
the sacral division, e. g., the distribution to the bladder, may
be in abeyance, while another part, e. g., the distribution to the
rectum, is active, illustrates again the directive discharge of
impulses which has been previously described as characteristic of
the cranial and sacral portions of the autonomic system.
Like the cranial division, the sacral is engaged in internal service
to the body, in the performance of acts leading immediately to
greater comfort.
The Sympathetic Division Antagonistic To Both
The Cranial and the Sacral
As indicated in the foregoing description many of the viscera are
innervated both by the cranial or sacral part of the autonomic and
by the sympathetic. _When the mid-part meets either end-part in any
viscus their effects are antagonistic._ Thus the cranial supply
to the eye contracts the pupil, the sympathetic dilates it; the
cranial slows the heart, the sympathetic accelerates it; the sacral
contracts the lower part of the large intestine, the sympathetic
relaxes it; the sacral relaxes the exit from the bladder, the
sympathetic contracts it. These opposed effects are indicated in
Fig. 1 by + for contraction, acceleration or increased tone; and
by - for inhibition, relaxation, or decreased tone.[*]
*[Footnote: The vagus nerve, when artificially stimulated, has
a primary, brief inhibitory effect on the stomach and small
intestine; its main function, however, as already stated, is to
produce increased tone and contraction in these organs. This
double action of the vagus is marked thus, ∓, in Fig. 1.]
Sherrington has demonstrated that the setting of skeletal muscles
in opposed groups about a joint or system of joints--as in flexors
and extensors--is associated with an internal organization of the
central nervous system that provides for relaxation of one group of
the opposed muscles when the other group is made to contract. This
“reciprocal innervation of antagonistic muscles,” as Sherrington has
called it,[26] is thus a device for orderly action in the body. As
the above description has shown, there are peripheral oppositions
in the viscera corresponding to the oppositions between flexor and
extensor muscles. In all probability these opposed innervations of
the viscera have counterparts in the organization of neurones in the
central nervous system. Sherrington has noticed, and I can confirm
the observation, that even though the sympathetic supply to the eye
is severed and is therefore incapable of causing dilation of the
pupil, nevertheless the pupil dilates in a paroxysm of anger--due,
no doubt (because the response is too rapid to be mediated by the
blood stream), to central inhibition of the cranial nerve supply to
the constrictor muscles--i. e., an inhibition of the muscles which
naturally oppose the dilator action of the sympathetic. Pain, the
major emotions--fear and rage--and also intense excitement, are
manifested in the activities of the sympathetic division. When in
these states impulses rush out over the neurones of this division
they produce all the changes typical of sympathetic excitation,
such as dilating the pupils, inhibiting digestion, causing pallor,
accelerating the heart, and various other well-known effects. The
impulses of the sympathetic neurones, as indicated by their dominance
over the digestive process, are capable of readily overwhelming
the conditions established by neurones of the cranial division of
the autonomic system.
Neurones of the Sympathetic Division and Adrenal Secretion
Have the Same Action
Lying anterior to each kidney is a small body--the adrenal gland.
It is composed of an external portion or cortex, and a central
portion or medulla. From the medulla can be extracted a substance,
called variously suprarenin, adrenin, epinephrin or “adrenalin,”[*]
which, in extraordinarily minute amounts, affects the structures
innervated by the sympathetic division of the autonomic system
precisely as if they were receiving nervous impulses. For example,
when adrenin is injected into the blood, it will cause pupils to
dilate, hairs to stand erect, blood vessels to be constricted,
the activities of the alimentary canal to be inhibited, and sugar
to be liberated from the liver. These effects are not produced
by action of the substance on the central nervous system, but by
direct action on the organ itself.[27] And the effects occur even
after the structures have been removed from the body and kept alive
artificially.
*[Footnote: The name “adrenalin” is proprietary. “Epinephrin”
and “adrenin” have been suggested as terms free from commercial
suggestions. As _adrenin_ is shorter and more clearly related to
the common adjectival form, _adrenal_, I have followed Schäfer in
using _adrenin_ to designate the substance produced physiologically
by the adrenal glands.]
The adrenals are glands of internal secretion, i. e., like the
thyroid, parathyroid, and pituitary glands, for example; they have
no connection with the surface of the body, and they give out into
the blood the material which they elaborate. The blood is carried
away from each of them by the lumbo-adrenal vein which empties either
into the renal vein or directly into the inferior vena cava just
anterior to the openings of the renal veins. The adrenal glands are
supplied by preganglionic fibres of the autonomic group,[28] shown
in solid line in Fig. 1. This seems an exception to the general
rule that gland cells have an outlying neurone between them and
the neurones of the central nervous system. The medulla of the
adrenal gland, however, is composed of modified nerve cells, and
may therefore be regarded as offering exceptional conditions.
The foregoing brief sketch of the organization of the autonomic
system brings out a number of points that should be of importance
as bearing on the nature of the emotions which manifest themselves
in the operations of this system. Thus it is highly probable that
the sympathetic division, because arranged for diffuse discharge,
is likely to be brought into activity as a whole, whereas the
sacral and cranial divisions, arranged for particular action on
separate organs, may operate in parts. Also, because antagonisms
exist between the middle and either end division of the autonomic,
affective states may be classified according to their expression in
the middle or an end division and these states would be, like the
nerves, antagonistic in character. And finally, since the adrenal
glands are innervated by autonomic fibres of the mid-division,
and since adrenal secretion stimulates the same activities that
are stimulated nervously by this division, it is possible that
disturbances in the realm of the sympathetic, although initiated
by nervous discharge, are automatically augmented and prolonged
through chemical effects of the adrenal secretion.
REFERENCES
[Footnote 21: Cannon: The American Journal of Psychology, 1914,
xxv, p. 257.]
[Footnote 22: For a summary of his studies of the organization of
the autonomic system, see Langley: Ergebnisse der Physiologie,
Wiesbaden, 1903, ii², p. 818.]
[Footnote 23: See Cannon: American Journal of Physiology, 1905,
xiii, p. xxii.]
[Footnote 24: See Sherrington: The Integrative Action of the Nervous
System, New York, 1909, p. 19.]
[Footnote 25: Langley and Anderson: Journal of Physiology, 1895,
xix, see pp. 85, 122.]
[Footnote 26: Sherrington: _Loc. cit._, p. 90.]
[Footnote 27: Elliott: Journal of Physiology, 1905, xxxii, p. 426.]
[Footnote 28: See Elliott: Journal of Physiology, 1913, xlvi, p.
289 ff.]
CHAPTER III
METHODS OF DEMONSTRATING ADRENAL SECRETION
AND ITS NERVOUS CONTROL
As stated in the first chapter, the inhibition of gastric secretion
produced by great excitement long outlasts the presence of the object
which evokes the excitement. The dog that was enraged by seeing a
cat for five minutes secreted only a few drops of gastric juice
during the next fifteen minutes. Why did the state of excitation
persist so long after the period of stimulation had ended? This
question, which presented itself to me while reading Bickel and
Sasaki’s paper, furnished the suggestion expressed at the close of
the last chapter, that the excitement might provoke a flow of adrenal
secretion, and that the changes originally induced in the digestive
organs by nervous impulses might be continued by circulating
adrenin. The prolongation of the effect might be thus explained.
Whether that idea is correct or not has not been tested. Its chief
service was in leading to an enquiry as to whether the adrenal
glands are in fact stimulated to action in emotional excitement.
The preganglionic fibres passing to the glands are contained in the
splanchnic nerves. What is the effect of splanchnic stimulation?
The Evidence that Splanchnic Stimulation
Induces Adrenal Secretion
It was in 1891 that Jacobi[29] described nerve fibres derived
from the splanchnic trunks which were distributed to the adrenal
glands. Six years later Biedl[30] found that these nerves conveyed
vasodilator impulses to the glands, and he suggested that they
probably conveyed also secretory impulses. Evidence in support of
this suggestion was presented the following year by Dreyer,[31] who
demonstrated that electrical excitation of the splanchnic nerves
produced in the blood taken from the adrenal veins an increased
amount of a substance having the power of raising arterial blood
pressure, and that this result was independent of accompanying
changes in the blood supply to the glands. The conclusion drawn
by Dreyer that this substance was adrenin has been confirmed in
various ways by later observers. Tscheboksaroff[32] repeated
Dreyer’s procedure and found in blood taken from the veins after
splanchnic stimulation evidences of the presence of adrenin that
were previously absent. Asher[33] observed a rise of blood pressure
when the glands were stimulated in such a manner as not to cause
constriction of the arteries--the rise was therefore assumed to be
due to secreted adrenin. Dilation of the pupil was used by Meltzer
and Joseph[34] to prove secretory action of the splanchnics on the
adrenal glands; they found that stimulation of the distal portion
of the cut splanchnic nerve caused the pupil to enlarge--an effect
characteristic of adrenin circulating in the blood. Elliott[35]
repeated this procedure, but made it a more rigorous proof of
internal secretion of the adrenals by noting that the effect failed
to appear if the gland on the stimulated side was removed. Additional
proof was brought by myself and Lyman[36] when we found that the
typical drop in arterial pressure produced in cats by injecting small
amounts of adrenin could be exactly reproduced by stimulating the
splanchnic nerves after the abdominal blood vessels, which contract
when these nerves are excited, were tied so that no changes in them
could occur to influence the rest of the circulation.
The problem of splanchnic influence on the adrenal glands Elliott
attacked by a still different method. Using, as a measure, the
graded effects of graded amounts of adrenin on blood pressure, he
was able to assay the quantity of adrenin in adrenal glands after
various conditions had been allowed to prevail. The tests were made
on cats. In these animals each adrenal gland is supplied only by
the splanchnic fibres of its own side, and the two glands normally
contain almost exactly the same amount of adrenin. Elliott[37]
found that when the gland on one side was isolated by cutting its
splanchnic supply, and then impulses were sent along the intact
nerves of the other side, either by disturbing the animal or by
artificial excitation of the nerves, the gland to which these
fibres reached invariably contained less adrenin, often very much
less, than the isolated gland. Results obtained by the method
employed by Elliott have been confirmed with remarkable exactness
in results obtained by Folin, Denis and myself,[38] using a highly
sensitive color test after adding the gland extract to a solution
of phosphotungstic acid.
All these observations, with a variety of methods, and by a
respectable number of reliable investigators, are harmonious in
bringing proof that artificial stimulation of the nerves leading to
the adrenal glands will induce secretory activity in the adrenal
medulla, and that in consequence adrenin will be increased in the
blood. The fact is therefore securely established that in the body
a mechanism exists by which these glands can be made to discharge
this peculiar substance promptly into the circulation.
The Question of Adrenal Secretion in Emotional Excitement
As we have already seen, the phenomena of a great emotional
disturbance in an animal indicate that sympathetic impulses dominate
the viscera. When, for example, a cat becomes frightened, the pupils
dilate, the activities of the stomach and intestines are inhibited,
the heart beats rapidly, the hairs of the back and tail stand
erect--from one end of the animal to the other there are abundant
signs of nervous discharges along sympathetic courses. Do not the
adrenal glands share in this widespread subjugation of the viscera
to sympathetic control?
This question, whether the common excitements of an animal’s life
might be capable of evoking a discharge of adrenin, was taken up by
D. de la Paz and myself in 1910. We made use of the natural enmity
between two laboratory animals, the dog and the cat, to pursue our
experiments. In these experiments the cat, fastened in a comfortable
holder (the holder already mentioned as being used in X-ray studies
of the movements of the alimentary canal), was placed near a barking
dog. Some cats when thus treated showed almost no signs of fear;
others, with scarcely a movement of defense, presented the typical
picture. In favorable cases the excitement was allowed to prevail
for five or ten minutes, and in a few cases longer. Samples of
blood were taken within a few minutes before and after the period.
The Method of Securing Blood from Near the Adrenal Veins
The blood was obtained from the inferior vena cava anterior to
the opening of the adrenal veins, i. e., at a point inside the
body near the level of the notch at the lower end of the sternum.
To get the blood so far from the surface without disturbing the
animal was at first a difficult problem. We found, however, that by
making anesthetic with ethyl chloride the skin directly over the
femoral vein high in the groin, the vein could be quickly bared,
cleared of connective tissue, tied, and opened without causing any
general disturbance whatever. A long, fine, flexible catheter (2.4
millimeters in diameter) which had previously been coated with
vaseline inside and out, to lubricate it and to delay the clotting
of blood within it, was now introduced into the opening in the
femoral vein, thence through the iliac and on into the inferior
cava to a point near the level of the sternal notch. A thread
tied around this tube where, after being inserted to the proper
distance, it disappeared into the femoral vein, marked the extent of
insertion, and permitted a later introduction to the same extent.
This slight operation--a venesection, commonly practised on our
ancestors--consumed only a few minutes, and as the only possibility
of causing pain was guarded against by local anesthesia, the animal
remained tranquil throughout. Occasionally it was necessary to
stroke the cat’s head gently to keep her quiet on the holder, and
under such circumstances I have known her to purr during all the
preparations for obtaining the blood, and while the blood was being
taken.
The blood (3 or 4 cubic centimeters) was slowly drawn through the
catheter into a clean glass syringe. Care was taken to avoid any
marked suction such as might cause collapse of the vein near the
inner opening of the tube. As soon as the blood was secured, the
catheter was removed and the vein tied loosely, to prevent bleeding.
The blood was at once emptied into a beaker, and the fibrin whipped
from it by means of fringed rubber tubing fitted over a glass rod.
Since this defibrinated blood was obtained while the animal was
undisturbed, it was labelled “quiet blood.”
The animal was then exposed to the barking dog, as already described,
and immediately thereafter blood was again removed, from precisely
the same region as before. This sample, after being defibrinated,
was labelled “excited blood.” The two samples, the “quiet” and
the “excited,” both obtained in the same manner and subsequently
treated in the same manner, were now tested for their content of
adrenin.
The Method of Testing the Blood for Adrenin
It was desirable to use as a test tissues to which the blood was
naturally related. As will be recalled, adrenin affects viscera
even after they have been removed from the body, just as if they
were receiving impulses via sympathetic fibres, and further, that
sympathetic fibres normally deliver impulses which cause contraction
of the internal genitals and relaxation of the stomach and
intestines. The uterus has long been employed as a test for adrenin,
the presence of which it indicates by increased contraction. That
isolated strips of the longitudinal muscle of the intestine, which
are contracting rhythmically, are characteristically inhibited by
adrenin in dilutions of 1 part in 20 millions, had been shown by
Magnus in 1905. Although, previous to our investigation in 1910,
this extremely delicate reaction had not been used as a biological
signal for adrenin, it possesses noteworthy advantages over other
methods. The intestine is found in all animals and not in only
half of them, as is the uterus; it is ready for the test within a
few minutes, instead of the several hours said to be required for
the best use of the uterus preparation;[39] and it responds by
relaxing. This last characteristic is especially important, for
in defibrinated blood there are, besides adrenin, other substances
capable of causing contraction of smooth muscle,[40] and liable
therefore to lead to erroneous conclusions when a structure which
responds by contracting, such as uterus or artery, is used to prove
whether adrenin is present. On the other hand, substances producing
relaxation of smooth muscle are few, and are unusual in blood.[41]
We used, therefore, the strip of intestinal muscle as an indicator.
Later Hoskins[42] modified our procedure by taking, instead of the
strip, a short segment of the rabbit intestine. The segment is not
subjected to danger of injury during its preparation, and when fresh
it is almost incredibly sensitive. It may be noticeably inhibited
by adrenin, 1 part in 200 millions!
The strip, or the intestinal segment, was suspended between minute
wire pincers (_serres fines_) in a cylindrical chamber 8 millimeters
in diameter and 5 centimeters deep. By a thread attached to the
lower serre fine the preparation was drawn into the chamber, and was
held firmly; by the upper one it was attached to the short end of
a writing lever (see Fig. 2). When not exposed to blood, the strip
was immersed in a normal solution of the blood salts (Ringer’s).
The blood or the salt solution could be quickly withdrawn from or
introduced into the chamber, without disturbing the muscle, by
means of a fine pipette passed down along the inner surface. The
chamber and its contents, the stock of Ringer’s solution, and the
samples of “quiet” and “excited” blood were all surrounded by a
large volume of water kept approximately at body temperature (37°
C.). Through the blood or the salt solution in the chamber oxygen
was passed in a slow but steady stream of bubbles. Under these
circumstances the strip will live for hours, and will contract
and relax in a beautifully regular rhythm, which may be recorded
graphically by the writing lever.
[Illustration: Figure 2.--Diagram of the arrangements for recording
contractions of the intestinal muscle.]
The first effect of surrounding the muscle with blood, whether
“quiet” or “excited,” was to send it into a strong contraction which
might persist, sometimes with slight oscillations, for a minute or
two (see Figs. 4 and 5). After the initial shortening, the strip,
if in quiet blood soon began to contract and relax rhythmically
and with each relaxation to lengthen more, until a fairly even base
line appeared in the written record. At this stage the addition of
fresh “quiet” blood usually had no effect, even though the strip
were washed once with Ringer’s solution before the second portion
of the blood was added. For comparison of the effects of “quiet”
and “excited” blood on the contracting strip, the two samples were
each added to the muscle immediately after the Ringer’s solution
had been removed, or they were applied to the muscle alternately
and the differences in effect then noted. The results obtained by
these methods are next to be presented.
REFERENCES
[Footnote 29: Jacobi: Archiv für experimentelle Pathologie und
Pharmakologie, 1891, xxix, p. 185.]
[Footnote 30: Biedl: Archiv für die gesammte Physiologie, 1897,
lxvii, pp. 456, 481.]
[Footnote 31: Dreyer: American Journal of Physiology, 1898-99, ii,
p. 219.]
[Footnote 32: Tscheboksaroff: Archiv für die gesammte Physiologie,
1910, cxxxvii, p. 103.]
[Footnote 33: Zeitschrift für Biologie, 1912, lviii, p. 274.]
[Footnote 34: Meltzer and Joseph: American Journal of Physiology,
1912, xxix, p. xxxiv.]
[Footnote 35: Elliott: Journal of Physiology, 1912, xliv, p. 400.]
[Footnote 36: Cannon and Lyman: American Journal of Physiology,
1913, xxxi, p. 377.]
[Footnote 37: Elliott: Journal of Physiology, 1912, xliv, p. 400.]
[Footnote 38: Folin, Cannon and Denis: Journal of Biological
Chemistry, 1913, xiii, p. 477.]
[Footnote 39: Fraenkel: Archiv für experimentelle Pathologie und
Pharmakologie, 1909, lx, p. 399.]
[Footnote 40: See O’Connor: Archiv für die experimentelle Pathologie
und Pharmakologie, 1912, lxvii, p. 206.]
[Footnote 41: Grutzner: Ergebnisse der Physiologie, 1904, iii²,
p. 66; Magnus: _Loc. cit._, p. 69.]
[Footnote 42: Hoskins: Journal of Pharmacology and Experimental
Therapeutics, 1911, iii, p. 95.]
CHAPTER IV
ADRENAL SECRETION IN STRONG EMOTIONS AND PAIN
If the secretion of adrenin is increased in strong emotional states
and in pain, that constitutes a fact of considerable significance,
for, as already mentioned, adrenin is capable of producing many
of the bodily changes which are characteristically manifested in
emotional and painful experiences. It is a matter of prime importance
for further discussion to determine whether the adrenal glands are
in fact roused to special activity in times of stress.
The Evidence that Adrenal Secretion Is Increased in
Emotional Excitement
That blood from the adrenal veins causes the relaxation of intestinal
muscle characteristic of adrenal extract or adrenin is shown in
Fig. 3. The muscle was originally beating in blood which contained
no demonstrable amount of adrenal secretion; this inactive blood
was replaced by blood from the adrenal veins, obtained after quick
etherization. Etherization, it will be recalled, is accompanied by
a “stage of excitement.” Relaxation occurred almost immediately (at
_b_). Then the rhythm was renewed in the former blood, and thereupon
the muscle was surrounded with blood from the vein leading away
from the left kidney, i. e., blood obtained from the same animal
and under the same conditions as the adrenal blood, but from a
neighboring vein. No relaxation occurred. By this and other similar
tests the reliability of the method was proved.
[Illustration: Figure 3.--Intestinal muscle beating in inactive
blood, which was withdrawn from the chamber at _a_. Blood from the
_adrenal_ vein of an animal excited by etherization was substituted
at _b_, and withdrawn at _c_. Contractions were restored in the
original inactive blood which was removed at _d_. Blood from the
_renal_ vein (same animal) was added at _e_.
In this and subsequent records time is marked in half minutes.]
In no instance did blood from the inferior vena cava of the quiet
normal animal produce relaxation. On the other hand, blood from the
animal after emotional excitement showed more or less promptly the
typical relaxation. In Fig. 4 is represented the record of intestinal
muscle which was beating regularly in Ringer’s solution. At _a_ the
Ringer’s solution was removed, and at _b_ “excited” blood was added;
after the preliminary shortening, which, as already stated, occurs
at the first immersion in blood, the muscle lengthened gradually
into complete inhibition. At _c_ the “excited” blood was removed,
and at _d_ “quiet” blood was added in its place. The muscle at
once began fairly regular rhythmic beats. At _e_ the “quiet” blood
was removed, and at _f_ the “excited” blood was again applied. The
muscle lengthened almost immediately into an inhibited state. In
this instance the “excited” blood was taken after the cat had been
barked at for about fifteen minutes.
[Illustration: Figure 4.--Alternate application of “excited” blood
(at _b_ and _f_) and “quiet” blood (at _d_), from the same animal,
to intestinal muscle initially beating in Ringer’s solution.]
The increase of effect with prolongation of the period of excitement
is shown in Fig. 5. _A_ is the record of contractions after the
muscle was surrounded with “quiet” blood serum. _B_ shows the
gradual inhibition which occurred when the muscle was surrounded
with defibrinated blood taken when the animal had been excited
eleven minutes. And _C_ is the record of rapid inhibition after
fifteen minutes of excitement. In other instances the effect was
manifested merely by a lowering of the tonus of the muscle, and a
notable slowing of the beats, without, however, a total abolition
of them.
[Illustration: Figure 5.--The effect of prolonging the
excitement. _A_, the record in “quiet” serum; _B_, in defibrinated
blood after eleven minutes of excitement; and _C_, in serum after
fifteen minutes of excitement.]
The inference that this inhibition of contraction of the intestinal
muscle is due to an increased amount of adrenal secretion in the
“excited” blood de la Paz and I justified on several grounds:
(1) The inhibition was produced by “excited” blood from the inferior
vena cava anterior to the mouths of the adrenal veins, when blood
from the femoral vein, taken at the same time, had no inhibitory
influence. Since blood from the femoral vein is typical of the
cava blood below the entrance of the kidney veins, the conclusion
is warranted that the difference of effect of the two samples of
blood is not due to any agent below the kidneys. But that blood
from the kidneys does not cause the relaxation is shown in Fig. 3.
The only other structures which could alter the blood between the
two points at which it was taken are the adrenal glands, and the
material secreted by them would produce precisely the inhibition
of contraction which was in fact produced.
(2) If in ether anesthesia the blood vessels leading to and from the
adrenal glands are first carefully tied, and then the glands are
removed, excitement four or five hours later, before the weakness
that follows the removal has become prominent, does not alter the
blood so that the typical inhibition occurs (see Fig. 6). Thus,
although the animal shows all the characteristic signs of sympathetic
stimulation, the blood, in the absence of the adrenals, remains
unchanged.
[Illustration: Figure 6.--Failure of the cava blood (added at
_a_) to produce inhibition when excitement has occurred after
removal of the adrenal glands. The muscle later proved sensitive
to adrenin in blood in the ratio 1:1,000,000.]
(3) As already shown, sometimes the effect produced by the “excited”
blood was prompt inhibition, sometimes the inhibition followed only
after several beats, and sometimes a slowing and shortening of
contractions, with a lower tone, were the sole signs of the action
of adrenin. All these degrees of relaxation can be duplicated by
adding to inactive blood varying amounts of adrenin. Fig. 7 shows
the effects, on a somewhat insensitive muscle preparation, of adding
adrenin, 1:1,000,000 (A), 1:2,000,000 (B), and 1:3,000,000 (C), to
different samples of blood previously without inhibitory influence.
These effects of adrenin and the effects produced by blood taken
near the opening of the adrenal veins are strikingly analogous.
[Illustration: Figure 7.--Effect of adding adrenin 1:1,000,000 (A),
1:2,000,000 (B), and 1:3,000,000 (C), to formerly inactive blood.
In each case _a_ marks the moment when the quiet blood was removed,
and _b_, the time when the blood with adrenin was added.]
(4) Embden and v. Furth[43] have reported that 0.1 gram of suprarenin
chloride disappears almost completely in two hours if added to
200 cubic centimeters of defibrinated beef blood, and the mixture
constantly aerated at body temperature. “Excited” blood which
produces inhibition loses that power on standing in the cold for
twenty-four hours, or on being kept warm and agitated with bubbling
oxygen. This change is illustrated in Fig. 8; the power of the
“excited” blood to inhibit the contractions of the intestinal muscle
when record _A_ was written was destroyed after three hours of
exposure to bubbling oxygen, as shown by record _B_. The destruction
of adrenin and the disappearance of the effect which adrenin would
produce are thus closely parallel.
[Illustration: Figure 8.--The effect of bubbling oxygen through
active blood. A, relaxation after active blood applied at _a_; B,
failure of relaxation when the same blood, oxygenated three hours,
was applied to a fresh strip at _b_.]
All these considerations, taken with the proof that sympathetic
impulses increase secretion of the adrenal glands, and taken also
with the evidence that, during such emotional excitement as was
employed in these experiments, signs of sympathetic discharges
appeared throughout the animal from the dilated pupil of the eye to
the standing hairs of the tail-tip, led us to the conclusions that
the characteristic action of adrenin on intestinal muscle was in
fact, in our experiments, due to secretion of the adrenal glands,
and that that secretion is increased in great emotion.
The Evidence that Adrenal Secretion is Increased by
“Painful” Stimulation
As mentioned in the first chapter, stimulation of sensory fibres in
one of the larger nerve trunks is known to result in such nervous
discharges along sympathetic paths as to produce marked inhibition
of digestive processes. Other manifestations of sympathetic
innervations--e. g., contraction of arterioles, dilation of pupils,
erection of hairs--are also demonstrable. And since the adrenal
glands are stimulated to activity by sympathetic impulses, it
was possible that they would be affected as are other structures
supplied with sympathetic fibres, and that they would secrete in
greater abundance when sensory nerves were irritated.
The testing of this possibility was undertaken by Hoskins and
myself in 1911. Since bodily changes from “painful” stimulation can
in large degree be produced in an anesthetized animal, without,
however, an experience of pain by the animal, it was possible to
make the test quite simply. The sensory stimulus was a rapidly
interrupted induced current applied to the sciatic nerve. The current
was increased in strength as time passed, and thus the intensity
of the effect, indicated by continuous dilation of the pupils, was
maintained. There was no doubt that such stimulation would have
caused very severe pain if the animal had not been anesthetized.
Indeed, the stimulus used was probably much stronger than would
be necessary to obtain a positive result in the absence of the
anesthetic (urethane), which markedly lessens the irritability of
visceral nerve fibres.[44] In different instances the stimulation
lasted from three to six minutes. Throughout the period there was
markedly increased rapidity and depth of breathing.
As Fig. 9 shows, the normal blood, removed from the vena cava before
stimulation, caused no inhibition of the beating segment, whereas
that removed afterwards produced a deep relaxation. Hoskins and I
showed that the increased respiration which accompanies “painful”
stimulation does not augment adrenal activity. We concluded,
therefore, that when a sensory trunk is strongly excited the adrenal
glands are reflexly stimulated, and that they pour into the blood
stream an increased amount of adrenin.
[Illustration: Figure 9.--Intestinal muscle beating in normal
vena cava blood, removed at 1 and renewed at 2. At 3 normal blood
removed. At 4 contraction inhibited by vena cava blood drawn
after sensory stimulation; at 5 removed. At 6 Ringer’s solution
substituted.]
Confirmation of Our Results by Other Observers
The foregoing experiments and conclusions were reported in 1911.
In 1912, Elliott[45] brought confirmatory evidence by use of a
method quite different from ours. As previously stated, he studied
the effects of experimental procedures on adrenal secretion by a
careful comparative quantitative assay of the adrenin content of the
glands when one gland was isolated from the central nervous system
and the other left connected. He took advantage of the action of
morphia and of the substance Β-tetrahydronaphthylamine in evoking
in cats all the appearances of great fright. After the animals
had thus been “frightened,” he found that the adrenal gland which
was still connected with the spinal cord was much depleted of its
adrenin content compared with the other, isolated gland. And he
observed, further, that animals newly brought to the laboratory,
and evidently disturbed by the strangeness of their surroundings,
had a considerably smaller amount of adrenin in their glands than
other animals grown accustomed to the situation. Elliott also
observed that prolonged excitation of a sensory nerve, such as the
great sciatic, may cause the adrenin largely to disappear from the
gland still connected with the central nervous system and subjected,
therefore, to reflex influences.
Our conclusions have also been confirmed more recently (1913) by
Hitchings, Sloan and Austin,[46] working in Crile’s laboratory in
Cleveland. They used the same method which we had used to obtain
blood and to test for adrenin, and found that after great fear and
rage had been induced in a cat by the attempt of a muzzled dog to
fight it, the adrenin reaction was clearly demonstrable. And just
as we had noted that the reaction did not occur if the adrenal
glands had been removed, they showed that it did not occur if the
nervous connections with the spinal cord were previously severed.
The logic of all these experiments may be briefly summed up. That
the adrenal glands are subject to splanchnic influence has been
demonstrated anatomically and by the physiological effects of their
secretion after artificial stimulation of the splanchnic nerves.
Impulses are normally sent along these nerves, in the natural
conditions of life, when animals become greatly excited, as in
fear and rage and pain. There is every probability, therefore, that
these glands are stimulated to extra secretion at such times. Both
by an exceedingly delicate biological test (intestinal muscle) and
by an examination of the glands themselves, clear evidence has been
secured that in pain and deep emotion the glands do, in fact, pour
out an excess of adrenin into the circulating blood.
Here, then, is a remarkable group of phenomena--a pair of glands
stimulated to activity in times of strong excitement and by such
nerve impulses as themselves produce at such times profound changes
in the viscera; and a secretion given forth into the blood stream
by these glands, which is capable of inducing by itself, or of
augmenting, the nervous influences which induce the very changes in
the viscera which accompany suffering and the major emotions. What
may be the significance of these changes, occurring when conditions
of pain and great excitement--experiences common to animals of
most diverse types and probably known to their ancestors for ages
past--lay hold of the bodily functions and determine the instinctive
responses?
Certain remarkable effects of injecting adrenin into the blood have
for many years been more or less well recognized. For example, when
injected it causes liberation of sugar from the liver into the
blood stream. It relaxes the smooth muscle of the bronchioles. Some
old experiments indicated that it acts as an antidote for muscular
fatigue. It alters the distribution of the blood in the body, driving
it from the abdominal viscera into the heart, lungs, central nervous
system and limbs. And there was some evidence that it renders more
rapid the coagulation of the blood. There may be other activities
of adrenin not yet discovered--it may coöperate with the products
of other glands of internal secretion. And other glands of internal
secretion may be stimulated by sympathetic impulses. But we were
not concerned with these possibilities. We wished to know whether
the adrenin poured out in pain and emotional excitement produced
or helped to produce the same effects that follow the injection of
adrenin. Our later researches were concerned with answers to this
question.
REFERENCES
[Footnote 43: Embden and v. Furth: Hofmeister’s Beiträge zur
chemischen Physiologie und Pathologie, 1904, iv, p. 423.]
[Footnote 44: Elliott: Journal of Physiology, 1905, xxxii, p. 448.]
[Footnote 45: Elliott: Journal of Physiology, 1912, xliv, p. 409.]
[Footnote 46: Hitchings, Sloan and Austin: Cleveland Medical Journal,
1913, xii, p. 686; see also Crile and Lower: Anoci-association,
Philadelphia, 1914, p. 56.]
CHAPTER V
THE INCREASE OF BLOOD SUGAR IN PAIN AND GREAT EMOTION
Sugar is the form in which carbohydrate material is transported in
organisms; starch is the storage form. In the bodies of animals
that have been well fed the liver contains an abundance of glycogen
or “animal starch,” which may be called upon in times of need.
At such times the glycogen is changed, and set free in the blood
as sugar. Ordinarily there is a small percentage of sugar in the
blood--from 0.06 to 0.1 per cent. When only this small amount is
present the kidneys are capable of preventing its escape in any
noteworthy amount. If the percentage rises to the neighborhood of
0.2-0.3 per cent, however, the sugar passes the obstacle set up by
the kidneys, and is readily demonstrable in the urine by ordinary
tests. The condition of “glycosuria,” therefore, may properly be
considered, in certain circumstances, as evidence of increased sugar
in the blood. The injection of adrenin can liberate sugar from the
liver to such an extent that glycosuria results. Does the adrenal
secretion discharged in pain and strong emotional excitement play
a rôle in producing glycosuria under such conditions?
In clinical literature scattered suggestions are to be found that
conditions giving rise to emotional states may be the occasion also
of more or less permanent glycosuria. Great grief and prolonged
anxiety during a momentous crisis have been regarded as causes of
individual instances of diabetes, and anger or fright has been
followed by an increase in the sugar excreted by persons who already
have the disease. Kleen[47] cites the instance of a German officer
whose diabetes and whose Iron Cross for valor both came from a
stressful experience in the Franco-Prussian War. The onset of the
disease in a man directly after his wife was discovered in adultery
is described by Naunyn;[48] and this author also mentions two cases
in his own practice--one started during the bombardment of Strassburg
(1870), the other started a few days after a companion had shot
himself. In cases of mental disease, also, states of depression have
been described accompanied by sugar in the urine. Schultze[49] has
reported that in these cases the amount of glycosuria is dependent
on the degree of depression, and that the greatest excretion of
sugar occurs in the fear-psychoses. Raimann[50] has reported that in
both melancholia and mania the assimilation limit of sugar may be
lowered. Similar results in the insane have recently been presented
by Mita,[51] and by Folin and Denis.[52] The latter investigators
found glycosuria in 12 per cent of 192 insane patients, most of
whom suffered from depression, apprehension, or excitement. And
Arndt[53] has observed glycosuria appearing and disappearing as
alcoholic delirium appeared and disappeared in his patients.
Although clinical evidence thus indicates an emotional origin of
some cases of diabetes and glycosuria, the intricacies of existence
and the complications of disease in human beings throw some doubt
on the value of that evidence. Both Naunyn[54] and Hirschfeld,
although mentioning instances of diabetes apparently due to an
emotional experience, urge a skeptical attitude toward such
statements. It is desirable, therefore, that the question of an
emotional glycosuria be tested under simpler and more controllable
conditions. “Emotional glycosuria” in experimental animals has
indeed been referred to by Waterman and Smit[55] and more recently
by Henderson and Underhill.[56] Both these references, however, are
based on the work of Böhm and Hoffmann,[57] reported in 1878.
Glycosuria From Pain
Böhm and Hoffmann found that cats, when bound to an operating
board, a tube inserted into the trachea (without anesthesia), and
in some instances a catheter inserted into the urethra through an
opening above the pubis, had in about half an hour an abundance
of sugar in the urine. In three determinations sugar in the blood
proved slightly above “normal” so long as sugar was appearing in
the urine, but returned to “normal” as the glycosuria disappeared.
Since they were able to produce the phenomenon by simply binding
animals to the holder, they called it “Fesselungsdiabetes.”
As possible causes of this glycosuria in bound animals, they
considered opening the trachea, cooling, and pain. The first two
they readily eliminated, and still they found sugar excreted. Pain
they could not obviate, and since, without binding the animals,
they caused glycosuria by merely stimulating the sciatic nerves,
they concluded that painful confinement was itself a sufficient
cause. Other factors, however, such as cooling and circulatory
disturbances, probably coöperated with pain, they believed, to
produce the result. Their observations on cats have been proved
true also of rabbits;[58] and recently it has been shown that an
operation involving some pain increases blood sugar in dogs.[59]
Temporary glycosuria has likewise been noted in association with
intense pain in human beings.
Inasmuch as Böhm and Hoffmann did not mention the emotional element
in discussing their results, and inasmuch as they admitted that
they could not obviate from their experimental procedure pain,
which they themselves proved was effective in causing glycosuria,
designating what they called “Fesselungsdiabetes” as “emotional
glycosuria” is not justified.
Emotional Glycosuria
The discovery that during strong emotion adrenal secretion is
increased, and the fact that injection of adrenin gives rise to
glycosuria, suggested that glycosuria might be called forth by
emotional excitement, and then that even without the painful element
of Böhm and Hoffmann’s experiments, sugar might be found in the
urine. The testing of this possibility was undertaken by A. T.
Shohl, W. S. Wright and myself in 1911.
Our first procedure was a repetition of Böhm and Hoffmann’s
experiments, freed from the factor of pain. The animals (cats) were
bound to a comfortable holder, which left the head unfastened. This
holder I had used hundreds of times in X-ray studies of digestion,
with many different animals, without causing any signs of even so
much as uneasiness. Just as in observations on the movements of the
alimentary canal, however, so here, the animals reacted differently
to the experience of being confined. Young males usually became quite
frantic, and with eyes wide, pupils dilated, pulse accelerated,
hairs of the tail more or less erect, they struggled, snarling and
growling, to free themselves. Females, on the contrary, especially
if elderly, were as a rule much more calm, and resignedly accepted
the novel situation.
According to differences in reaction the animals were left in the
holder for periods varying in length from thirty minutes to five
hours. In order to insure prompt urination, considerable quantities
of water were given by stomach tube at the beginning of the
experiment and in some cases again later. Arrangements were made for
draining the urine promptly, when the animal was on the holder or
when afterwards in a metal metabolism cage, into a glass receiver
containing a few drops of chloroform to prevent fermentation. The
diet in all cases consisted of customary raw meat and milk. In every
instance the urine was proved free from sugar before the animal
was excited.
In our series of observations twelve cats were used, and in every
one a well-marked glycosuria was developed. The shortest periods
of confinement to the holder which were effective were thirty and
forty minutes; the longest we employed, five hours. The average
time required to bring about a glycosuria was less than an hour
and a half; the average in seven of the twelve cases was less than
forty minutes. In all cases no sugar was found in the urine passed
on the day after the excitement.
The promptness with which the glycosuria developed was directly
related to the emotional state of the animal. Sugar was found early
in animals which early showed signs of being frightened or in a
rage, and much later in animals which took the experience more
calmly.
As cooling may result in increased sugar in the blood, and consequent
glycosuria, the rectal temperature was observed from time to time,
and it was found to vary so slightly that in these experiments it
was a wholly negligible factor. In one cat the rectal temperature
fell to 36° C. while the animal was bound and placed in a cold
room (about 2° C.) for fifty minutes, but no sugar appeared in the
urine.
Further evidence that the appearance of sugar in the urine may arise
purely from emotional excitement was obtained from three cats which
gave negative results when bound in the holder for varying periods
up to four hours. It was noteworthy that these animals remained calm
and passive in their confinement. When, however, they were placed,
separately, in a small wire cage, and were barked at by an energetic
little dog, that jumped at them and made signs of attack, the cats
became much excited, they showed their teeth, humped their backs,
and growled defiance. This sham fight was permitted to continue for
a half hour in each of the three cases. In each case the animal,
which after four hours of bondage had exhibited no glycosuria, now
had sugar in the urine. Pain, cooling, and bondage were not factors
in these experiments. The animal was either frightened or enraged
by the barking dog, and that excitement was attended by glycosuria.
The sugar excreted in the twenty-four hours which included the
period of excitement was determined by the Bertrand method.[60] It
ranged from 0.024 gram to 1.93 grams, or from 0.008 gram to 0.62
gram per kilo body weight, for the twenty-four hours’ quantity.
The presence of sugar in the urine may be used as an indication of
increased sugar in the blood, for unless injury has been done to
the cells of the kidneys, they do not permit sugar to escape until
the percentage in the blood has risen to a considerable degree.
Thus, though testing the urine reveals the instances of a high
content of blood sugar, it does not show the fine variations that
appear when the blood itself is examined. Recently Scott[61] has
concluded a thorough investigation of the variations of blood sugar
in cats, and has found that merely incidental conditions, producing
even mild excitement, as indicated by crying or otherwise, result
in a noticeable rise in the amount. Indeed, so sensitive is the
sugar-liberating mechanism that all the early determinations of the
“normal” content of sugar in blood which has been drawn from an
artery or vein in the absence of anesthesia, are of very doubtful
value. Certainly when care is taken to obtain blood suddenly from a
tranquil animal, the percentage (0.069, Scott; 0.088, Pavy) is much
less than when the blood is drawn without anesthesia (0.15, Böhm and
Hoffmann), or after light narcosis (0.282, Rona and Takahashi[62]).
Our observations on cats have since been found valid for rabbits.
Rolly and Oppermann, Jacobsen, and Hirsch and Reinbach[63] have
recently recorded that the mere handling of a rabbit preparatory
to operating on it will increase the percentage of blood sugar (in
some cases from 0.10 to 0.23 and 0.27 per cent). Dogs are said to be
much less likely to be disturbed by the nature of their surroundings
than are rabbits and cats. Nevertheless, pain and excitement are
such fundamental experiences in animals that without much doubt the
same mechanism is operative in all when these experiences occur.
Probably, just as the digestion of dogs is disturbed by strong
emotion, the blood sugar likewise is increased, for sympathetic
impulses occasion both changes.[*] Gib has given an account of a
bitch that became much agitated when shut up, and after such enforced
seclusion, but never otherwise, she excreted small quantities of
sugar in the urine.[64]
*[Footnote: Since the foregoing sentences were written Hirsch and
Reinbach have reported (Zeitschrift für physiologische Chemie,
1914, xci, p. 292) a “psychic hyperglycemia” in dogs, that resulted
from fastening the animals to a table. The blood sugar rose in
one instance from 0.11 to 0.14 per cent, and in another from 0.09
to 0.16 per cent.]
The results noted in these lower animals have been confirmed in
human beings. One of my former students, W. G. Smillie, found that
four of nine medical students, all normally without sugar in their
urine, had glycosuria after a hard examination, and only one of the
nine had glycosuria after an easier examination. The tests, which
were positive with Fehling’s solution, Nylander’s reagent, and also
with phenyl-hydrazine, were made on the first urine passed after
the examination. Furthermore, C. H. Fiske and I examined the urine
of twenty-five members of the Harvard University football squad
immediately after the final and most exciting contest of the season
of 1913, and found sugar in twelve cases. Five of these positive
cases were among substitutes not called upon to enter the game.
The only excited spectator of the Harvard victory whose urine was
examined also had a marked glycosuria, which on the following day
had disappeared.
Other tests made on students before and after important scholastic
examinations have been published by Folin, Denis and Smillie.[65]
Of thirty-four second-year medical students tested, one had sugar
before the examination as well as afterwards. Of the remaining
thirty-three, six, or 18 per cent, had small but unmistakable traces
of sugar in the urine passed directly following the ordeal. A
similar study was made on second-year students at a women’s college.
Of thirty-six students who had no sugar in the urine on the day
before, six, or 17 per cent, eliminated sugar with the urine passed
immediately after the examination.
From the foregoing results it is reasonable to conclude that just as
in the cat, dog, and rabbit, so also in man, emotional excitement
produces temporary increase of blood sugar.
The Rôle of the Adrenal Glands in Emotional Glycosuria
Since artificial stimulation of the splanchnic nerves produces
glycosuria,[66] and since major emotions, such as rage and fright,
are attended by nervous discharges along splanchnic pathways,
glycosuria as an accompaniment of emotional excitement would
naturally be expected to occur. To what extent the adrenal glands
which, as already mentioned, are stimulated to increased secretion by
excitement, might play a part in this process, has been in dispute.
Removal of these glands or cutting of the nerve fibres supplying
them, according to some observers,[67] prevents glycosuria after
puncture of the fourth ventricle of the brain (the “sugar puncture,”
which typically induces glycosuria) and also after stimulation of the
splanchnics.[68] On the other hand, Wertheimer and Battez[69] have
stated that removal of the glands does not abolish the effects of
sugar puncture in the cat. It was questionable, therefore, whether
removal of the adrenal glands would affect emotional glycosuria.
Evidence on this point I secured with Shohl and Wright in
observations on three animals in which the adrenals were removed
aseptically under ether. The animals selected had all become quickly
excited on being bound to the holder, and had manifested glycosuria
after about an hour of confinement. In the operation, to avoid
discharge of adrenin by handling, the adrenal veins were first
tied, and then the glands freed from their attachments and removed
as quickly and with as little manipulation as possible. In one cat
the entire operation was finished in twenty minutes. In two of the
cats a small catheter was introduced into the urethra through an
incision, so that the bladder could be emptied at any time.
In all three cases urine that was free from sugar was obtained
soon after the operation. Although the animals deprived of their
adrenals manifested a general lessening of muscular tone, they
still displayed much of their former rage or excitement when bound.
Indeed, one was more excited after removal of the adrenals than
before. That the animals might not be excessively cooled they were
kept warm with coverings or an electric heating pad. Although they
were now bound for periods from two to three times as long as the
periods required formerly to cause glycosuria, no trace of sugar
was found in the urine in any instance. The evidence thus secured
tends, therefore, to support the view that the adrenal glands
perform an important contributory rôle in the glycosuria resulting
from splanchnic stimulation.
Possibly the emotional element is in part accountable for the
glycosuria observed after painful stimulation, but conditions
causing pain alone will reasonably explain it. As we have already
seen, strong stimulation of sensory fibres causes the discharge of
impulses along the splanchnic nerves, and incidentally calls forth an
increased secretion of the adrenal glands. In glycosuria resulting
from painful stimulation, as well as in emotional glycosuria, the
adrenal glands may be essential factors.
Later the evidence will be given that sugar is the optimum source
of muscular energy. In passing, we may note that the liberation
of sugar at a time when great muscular exertion is likely to be
demanded of the organism may be interpreted as a highly interesting
instance of biological adaptation.
REFERENCES
[Footnote 47: Kleen: On Diabetes Mellitus and Glycosuria,
Philadelphia, 1900, pp. 22, 37-39.]
[Footnote 48: Naunyn: Der Diabetes Mellitus, Vienna, 1898, p. 72.]
[Footnote 49: Schultze: Verhandlungen der Gesellschaft deutscher
Naturforscher und Aerzte, Cologne, 1908, ii, p. 358.]
[Footnote 50: Zeitschrift für Heilkunde, 1902, xxiii, Abtheilung
iii, pp. 14, 19.]
[Footnote 51: Mita: Monatshefte für Psychiatrie und Neurologie,
1912, xxxii, p. 159.]
[Footnote 52: Folin, Denis and Smillie: Journal of Biological
Chemistry, 1914, xvii, p. 519.]
[Footnote 53: Arndt: Zeitschrift für Nervenheilkunde, 1897, x, p.
436.]
[Footnote 54: Naunyn: _Loc. cit._, p. 73; Hirschfeld: Die
Zuckerkrankheit, Leipzig, 1902, p. 45.]
[Footnote 55: Waterman and Smit: Archiv für die gesammte Physiologie,
1908, cxxiv, p. 205.]
[Footnote 56: Henderson and Underhill: American Journal of
Physiology, 1911, xxviii, p. 276.]
[Footnote 57: Böhm and Hoffmann: Archiv für experimentelle Pathologie
und Pharmakologie, 1878, viii, p. 295.]
[Footnote 58: Eckhard: Zeitschrift für Biologie, 1903, xliv, p.
408.]
[Footnote 59: Loewy and Rosenberg: Biochemische Zeitschrift, 1913,
lvi, p. 114.]
[Footnote 60: See Abderhalden: Handbuch der biochemischen
Arbeitsmethoden, Berlin, 1910, ii, p. 181.]
[Footnote 61: Scott: American Journal of Physiology, 1914, xxxiv,
p. 283.]
[Footnote 62: Cited by Scott: _Loc. cit._, p. 296.]
[Footnote 63: Rolly and Oppermann: Biochemische Zeitschrift, 1913,
xlix, p. 201. Jacobsen: _Ibid._, 1913, li, p. 449. Hirsch and
Reinbach: Zeitschrift für physiologische Chemie, 1913, lxxxvii, p.
122.]
[Footnote 64: Cited by Kleen: _Loc. cit._, p. 37.]
[Footnote 65: Folin, Denis and Smillie: _Loc. cit._, p. 520.]
[Footnote 66: See Macleod: American Journal of Physiology, 1907,
xix, p. 405, also for other references to literature.]
[Footnote 67: See Meyer: Comptes rendus de la Société de Biologie,
1906, lviii, p. 1123; Nishi: Archiv für experimentelle Pathologie
und Pharmakologie, 1909, lxi, p. 416.]
[Footnote 68: Gautrelet and Thomas: Comptes rendus de la Société
de Biologie, 1909, lxvii, p. 233; and Macleod: Proceedings of the
Society for Experimental Biology and Medicine, 1911, viii, p. 110
(true for left adrenal and left splanchnic).]
[Footnote 69: Wertheimer and Battez: Archives Internationales de
Physiologie, 1910, ix, p. 392.]
CHAPTER VI
IMPROVED CONTRACTION OF FATIGUED MUSCLE AFTER
SPLANCHNIC STIMULATION OF THE ADRENAL GLAND
In the older literature on the adrenal glands the deleterious effect
of their absence, or the beneficial effect of injected extracts,
on the contraction of skeletal muscle was not infrequently noted.
As evidence accumulated, however, tending to prove an important
relation between the extract of the adrenal medulla (adrenin) and
the sympathetic nervous system, the relations with the efficiency
of skeletal muscle began to receive less consideration.
The muscular weakness of persons suffering from diseased adrenals
(Addison’s disease) was well recognized before experimental work
on the glands was begun. Experiments on rabbits were reported in
1892 by Albanese,[70] who showed that muscles which were stimulated
after removal of the glands were much more exhausted than when
stimulated the same length of time in the same animal before the
removal. Similarly Boinet[71] reported, in 1895, that rats recently
deprived of their adrenals were much more quickly exhausted in a
revolving cage than were normal animals.
More direct evidence of the favorable influence of adrenal extract
on skeletal muscle was brought forward by Oliver and Schäfer.[72]
After injecting the extract subcutaneously into a frog they found
that the excised gastrocnemius muscle registered a curve of
contraction about 33 per cent higher and about 66 per cent longer
than the corresponding muscle not exposed to the action of the
extract. Similar prolongation of the muscle curve was observed
after injecting the extract intravenously into a dog. A beneficial
effect of adrenal extract on fatigued muscle, even when applied
to the solution in which the isolated muscle was contracting, was
claimed by Dessy and Grandis,[73] who studied the phenomenon in a
salamander.[*] Further evidence leading to the same conclusion was
offered in a discriminating paper by Panella.[74] He found that in
cold-blooded animals the active principle of the adrenal medulla
notably reënforced skeletal muscle, prolonging its ability to do
work, and improving its contraction when fatigued. In warm-blooded
animals the same effects were observed, but only after certain
experimental procedures, such as anesthesia and section of the bulb,
had changed them to a condition resembling the cold-blooded.
*[Footnote: These earlier investigations, in which an extract
of the entire gland was used, made no distinction between the
action of the medulla and that of the cortex. It may be that the
weakness following removal or disease of the adrenals is due to
absence of the cortex (see Hoskins and Wheelon: American Journal
of Physiology, 1914, xxxiv, p. 184). Such a possible effect,
however, should not be confused with the demonstrable influence
of injected adrenin (derived from the adrenal medulla alone) and
the similar effects from adrenal secretion caused by splanchnic
stimulation.]
The foregoing evidence indicates that removal of the adrenals has a
debilitating effect on muscular power, and that injection of extracts
of the glands has an invigorating effect. It seemed possible,
therefore, that increased secretion of the adrenal glands, whether
from direct stimulation of the splanchnic nerves or as a reflex
result of pain or the major emotions, might act as a dynamogenic
factor in the performance of muscular work. With this possibility in
mind L. B. Nice and I[75] first concerned ourselves in a research
which we conducted in 1912.
The general plan of the investigation consisted primarily in
observing the effect of stimulating the splanchnic nerves, isolated
from the spinal cord, on the contraction of a muscle whose nerve,
also isolated from the spinal cord, was rhythmically and uniformly
excited with break induction shocks. When a muscle is thus stimulated
it at first responds by strong contractions, but as time passes
the contractions become weaker, the degree of shortening of the
muscle becomes less, and in this state of lessened efficiency it
may continue for a long period to do work. The tired muscle which
is showing continuously and evenly its inability to respond as it
did at first, is said to have reached the “fatigue level.” This
level serves as an excellent basis for testing influences that may
have a beneficial effect on muscular performance, for the benefit
is at once manifested in greater contraction.
In the experimental arrangement which we used, only a connection
through the circulating blood existed between the splanchnic region
and the muscle--all nervous relations were severed. Any change in
muscular ability, therefore, occurring when the splanchnic nerve is
stimulated, must be due to an alteration in the quantity or quality
of the blood supplied to the laboring muscle.
Cats were used for most experiments, but results obtained with cats
were confirmed on rabbits and dogs. To produce anesthesia in the
cats and rabbits, and at the same time to avoid the fluctuating
effects of ether, urethane (2 grams per kilo body weight) was given
by a stomach tube. The animals were fastened back downward, over
an electric warming pad, to an animal holder. Care was taken to
maintain the body temperature at its normal level throughout each
experiment.
The Nerve-muscle Preparation
The muscle selected to be fatigued was usually the extensor of the
right hind foot (the _tibialis anticus_), though at times the common
extensor muscle of the digits of the same foot was employed. The
anterior tibial nerve which supplies these muscles was bared for
about two centimeters, severed toward the body, and set in shielded
electrodes, around which the skin was fastened by spring clips. Thus
the nerve could be protected, kept moist, and stimulated without
stimulation of neighboring structures. By a small slit in the skin
the tendon of the muscle was uncovered, and after a strong thread
was tied tightly about it, it was separated from its insertion. A
nerve-muscle preparation was thereby made which was still connected
with its proper blood supply. The preparation was fixed firmly to
the animal holder by thongs looped around the hock and the foot, i.
e., on either side of the slit through which the tendon emerged.
The thread tied to the tendon was passed over a pulley and down to
a pivoted steel bar which bore a writing point. Both the pulley
and this steel writing lever were supported in a rigid tripod. In
the earliest experiments the contracting muscle was made to lift
weights (125 to 175 grams); in all the later observations, however,
the muscle pulled against a spring attached below the steel bar.
The tension of the spring as the muscle began to lift the lever
away from the support was, in most of the experiments, 110 grams,
with an increase of 10 grams as the writing point was raised 4.5
millimeters. The magnification of the lever was 3.8.
The stimuli delivered to the anterior tibial nerve were, in most
experiments, single break shocks of a value barely maximal when
applied to the fresh preparation. The rate of stimulation varied
between 60 and 300 per minute, but was uniform in any single
observation. A rate which was found generally serviceable was 180
per minute.
Since the anterior tibial nerve contains fibres affecting blood
vessels, as well as fibres causing contraction of skeletal muscle,
the possibility had to be considered that stimuli applied to it might
disturb the blood supply of the region. Constriction of the blood
vessels would be likely to produce the most serious disturbance, by
lessening the blood flow to the muscle. The observations of Bowditch
and Warren,[76] that vasodilator rather than vasoconstrictor effects
are produced by single induction shocks repeated at intervals of
not more than five per second, reassured us as to the danger of
diminishing the blood supply, for the rate of stimulation in our
experiments never exceeded five per second and was usually two or
three. Furthermore, in using these different rates we have never
noted any result which could reasonably be attributed to a diminished
circulation.
The Splanchnic Preparation
The splanchnic nerves were stimulated in various ways. At first
only the left splanchnics in the abdomen were prepared. The nerves,
separated from the spinal cord, were placed upon shielded electrodes.
The form of electrodes which was found most satisfactory was that
illustrated in Fig. 10. The instrument was made of a round rod of
hard wood, bevelled to a point at one end, and grooved on the two
sides. Into the grooves were pressed insulated wires ending in
platinum hooks, which projected beyond the bevelled surface. Around
the rod was placed an insulating rubber tube which was cut out so
as to leave the hooks uncovered when the tube was slipped downward.
[Illustration: Figure 10.--The shielded electrodes used in
stimulating the splanchnic nerves. For description see text.]
In applying the electrodes the left splanchnic nerves were first
freed from their surroundings and tightly ligatured as close as
possible to their origin. By means of strong compression the
conductivity of the nerves was destroyed central to the ligature.
The electrodes were now fixed in place by thrusting the sharp end
of the wooden rod into the muscles of the back. This was so done
as to bring the platinum hooks a few millimeters above the nerves.
With a small seeker the nerves were next gently lifted over the
hooks, and then the rubber tube was slipped downward until it came
in contact with the body wall. Absorbent cotton was packed about
the lower end of the electrodes, to take up any fluid that might
appear; and finally the belly wall was closed with spring clips. The
rubber tube served to keep the platinum hooks from contact with the
muscles of the back and the movable viscera, while still permitting
access to the nerves which were to be stimulated. This stimulating
apparatus could be quickly applied, and, once in place, needed no
further attention. In some of the experiments both splanchnic nerves
were stimulated in the thorax. The rubber-covered electrode proved
quite as serviceable there as in the abdomen.
The current delivered to the splanchnic nerves was a rapidly
interrupted induced current of such strength that no effects of
spreading were noticeable. That splanchnic stimulation causes
secretion of the adrenal glands has been proved in many different
ways which have already been described (see p. 41).
The Effects of Splanchnic Stimulation on the
Contraction of Fatigued Muscle
When skeletal muscle is repeatedly stimulated by a long series of
rapidly recurring electric shocks, its strong contractions gradually
grow weaker until a fairly constant condition is reached. The record
then has an even top--the muscle has reached the “fatigue level.”
The effect of splanchnic stimulation was tried when the muscle had
been fatigued to this stage. The effect which was often obtained by
stimulating the left splanchnic nerves is shown in Fig. 11. In this
instance the muscle while relaxed supported no weight, and while
contracting lifted a weight of 125 grams. The rate of stimulation
was 80 per minute.
[Illustration: Figure 11.--Upper record, contraction of the
_tibialis anticus_, 80 times a minute, lifting a weight of 125
grams. Lower record, stimulation of the left splanchnic nerves,
two minutes. Time, half minutes.]
The muscle record shows a brief initial rise from the fatigue
level, followed by a drop, and that in turn by another, prolonged
rise. The maximum height of the record is 13.5 millimeters, an
increase of 6 millimeters over the height recorded before splanchnic
stimulation. Thus the muscle was performing for a short period 80
per cent more work than before splanchnic stimulation, and for a
considerably longer period exhibited an intermediate betterment of
its efficiency.
The First Rise in the Muscle Record
The brief first elevation in the muscle record when registered
simultaneously with arterial blood pressure is observed to occur at
the same time with the sharp initial rise in the blood-pressure
curve (see Fig. 12). The first sharp rise in blood pressure is due
to contraction of the vessels in the area of distribution of the
splanchnic nerves, for it does not appear if the alimentary canal
is removed, or if the celiac axis and the superior and inferior
mesenteric arteries are ligated. The betterment of the muscular
contraction is probably due directly to the better blood supply
resulting from the increased pressure, for if the adrenal veins are
clipped and the splanchnic nerves are stimulated, the blood pressure
rises as before and at the same time there may be registered a
higher contraction of the muscle.
[Illustration: Figure 12.--Top record, arterial blood pressure
with membrane manometer. Middle record, contractions of _tibialis
anticus_ loaded with 125 grams and stimulated 80 times a minute.
Bottom record, splanchnic stimulation (two minutes). Time, half
minutes.]
The Prolonged Rise in the Muscle Record
As Fig. 12 shows, the initial quick uplift in the blood-pressure
record is quickly checked by a drop. This rapid drop does not
appear when the adrenal veins are obstructed. A similar difference
in blood-pressure records has been noted before and after excision
of the adrenal glands. As Elliott,[77] and as Lyman and I[78] have
shown, this sharp drop after the first rise, and also the subsequent
elevation of blood pressure, are the consequences of liberation of
adrenal secretion into the circulation. Fig. 12 demonstrates that
the prolonged rise of the muscle record begins soon after this
characteristic drop in blood pressure.
If after clips have been placed on the adrenal veins so that no
blood passes from them, the splanchnic nerves are stimulated, and
later the clips are removed, a slight but distinct improvement in
the muscular contraction occurs. As in the experiments of Young
and Lehmann,[79] in which the adrenal veins were tied for a time
and then released, the release of the blood which had been pent
in these veins was quickly followed by a rise of blood pressure.
The volume of blood thus restored to circulation was too slight to
account for the rise of pressure. In conjunction with the evidence
that splanchnic stimulation calls forth adrenal secretion, the rise
may reasonably be attributed to that secretion. The fact should be
noted, however, that in this instance the prolonged improvement in
muscular contraction did not appear until the adrenal secretion
had been admitted to the general circulation.
Many variations in the improvement of activity in fatigued muscle
after splanchnic stimulation were noted in the course of our
investigation. The improvement varied in degree, as indicated by
increased height of the record. In some instances the height of
contraction was doubled--a betterment by 100 per cent; in other
instances the contraction after splanchnic stimulation was only a
small fraction higher than that preceding the stimulation; and in
still other instances there was no betterment whatever. Never,
in our experience, were the augmented contractions equal to the
original strong contractions of the fresh muscle.
The improvement also varied in degree as indicated by persistence of
effect. In some instances the muscle returned to its former working
level within four or five minutes after splanchnic stimulation
ceased (see Fig. 11); and in other cases the muscle continued
working with greater efficiency for fifteen or twenty minutes after
the stimulation.
The Two Factors: Arterial Pressure and Adrenal Secretion
The evidence just presented has shown that splanchnic stimulation
improves the contraction of fatigued muscle. Splanchnic stimulation,
however, has two effects--it increases general arterial pressure
and it also causes a discharge of adrenin from the adrenal glands.
The questions now arise--Does splanchnic stimulation produce the
improvement in muscular contraction by increasing the arterial
blood pressure and thereby flushing the laboring muscles with fresh
blood? Or does the adrenin liberated by splanchnic stimulation act
itself, specifically, to improve the muscular contraction? Or may
the two factors coöperate? These questions will be dealt with in
the next two chapters.
REFERENCES
[Footnote 70: Albanese: Archives Italiennes de Biologie, 1892,
xvii, p. 243.]
[Footnote 71: Boinet: Comptes rendus, Société de Biologie, 1895,
xlvii, pp. 273, 498.]
[Footnote 72: Oliver and Schäfer: Journal of Physiology, 1895, xviii,
p. 263. See also Radwánska, Anzeiger der Akademie, Krakau, 1910,
pp. 728-736. Reviewed in Zentralblatt für Biochemie und Biophysik,
1911, xi, p. 467.]
[Footnote 73: Dessy and Grandis: Archives Italiennes de Biologie,
1904, xli, p. 231.]
[Footnote 74: Panella: Archives Italiennes de Biologie, 1907,
xlviii, p. 462.]
[Footnote 75: Cannon and Nice: American Journal of Physiology,
1913, xxxii, p. 44.]
[Footnote 76: Bowditch and Warren: Journal of Physiology, 1886,
vii, p. 438.]
[Footnote 77: Elliott: Journal of Physiology, 1912, xliv, p. 403.]
[Footnote 78: Cannon and Lyman: American Journal of Physiology,
1913, xxxi, p. 376.]
[Footnote 79: Young and Lehmann: Journal of Physiology, 1908,
xxxvii, p. liv.]
CHAPTER VII
THE EFFECTS ON CONTRACTION OF FATIGUED MUSCLE OF
VARYING THE ARTERIAL BLOOD PRESSURE
That great excitement is accompanied by sympathetic innervations
which increase the contraction of the small arteries, render
unusually forcible the heart beat, and consequently raise arterial
pressure, has already been pointed out ( see p. 26). Indeed, the
counsel to avoid circumstances likely to lead to such excitement,
which is given to persons with hardened arteries or with weak
hearts, is based on the liability of serious consequences, either
in the heart or in the vessels, that might arise from an emotional
increase of pressure in these pathological conditions. That great
muscular effort also is accompanied by heightened arterial pressure
is equally well known, and is avoided by persons likely to be
injured by it. Both in excitement and in strong exertion the blood
is forced in large degree from the capacious vessels of the abdomen
into other parts of the body. In excitement the abdominal arteries
and veins are contracted by impulses from the splanchnic nerves.
In violent effort the diaphragm and the muscles of the belly wall
are voluntarily and antagonistically contracted in order to stiffen
the trunk as a support for the arms; and the increased abdominal
pressure which results forces blood out of that region and does not
permit reaccumulation. The general arterial pressure in man, as
McCurdy[80] has shown, may suddenly rise during extreme physical
effort, from approximately 110 millimeters to 180 millimeters of
mercury.
The Effect of Increasing Arterial Pressure
What effect the increase of arterial pressure, resulting from
excitement or physical strain, may have on muscular efficiency, has
received only slight consideration. Nice and I found there was need
of careful study of the relations between arterial pressure and
muscular ability, and, in 1913, one of my students, C. M. Gruber,
undertook to make clearer these relations.
The methods of anesthesia and stimulation used by Gruber were
similar to those described in the last chapter. The arterial blood
pressure was registered from the right carotid or the femoral
artery by means of a mercury manometer. A time marker indicating
half-minute intervals was placed at the atmospheric pressure level
of the manometer. And since the blood-pressure style, the writing
point of the muscle lever, and the time signal were all set in a
vertical line on the surface of the recording drum, at any given
muscular contraction the height of blood pressure was simultaneously
registered.
To increase general arterial pressure two methods were used: the
spinal cord was stimulated in the cervical region through platinum
electrodes, or the left splanchnic nerves were stimulated after the
left adrenal gland had been excluded from the circulation. This was
done in order to avoid any influence which adrenal secretion might
exert. It is assumed in these experiments that vessels supplying
active muscles would be actively dilated, as Kaufmann[81] has
shown, and would, therefore, in case of a general increase of blood
pressure, deliver a larger volume of blood to the area they supply.
The effects of increased arterial pressure are illustrated in Figs.
13, 14 and 15. In the experiment represented in Fig. 13, the rise
of blood pressure was produced by stimulation of the cervical cord,
and in Figs. 14 and 15 by stimulation of the left splanchnic nerves
after the left adrenal gland had been tied off.
The original blood pressure in Fig. 13 was 120 millimeters of
mercury. This was increased by 62 millimeters, with a rise of only
8.4 per cent in the height of contraction of the fatigued muscle.
[Illustration: Figure 13.--In this and the following records, the
upper curve indicates the blood pressure, the middle line muscular
contraction, and the lower line the time in 30 seconds (also zero
blood pressure.) Between the arrows the exposed cervical spinal
cord was stimulated.]
In Fig. 14 the original blood pressure was 100 millimeters of
mercury. By increasing this pressure 32 millimeters there resulted
simultaneous betterment of 9.8 per cent in the height of muscular
contraction. In Fig. 14 B the arterial pressure was raised 26
millimeters and the height of contraction increased correspondingly
7 per cent. In Fig. 14 C no appreciable betterment can be seen
although the blood pressure rose 18 millimeters.
[Illustration: Figure 14.--Stimulation of the left splanchnic
nerves (left adrenal gland tied off) during the periods indicated
by the arrows.]
In Fig. 15 the original blood pressure was low--68 millimeters of
mercury. This was increased in Fig. 15 A by 18 millimeters (the same
as in Fig. 14 C without effect), and there resulted an increase of
20 per cent in the height of contraction. In Fig. 15 B the pressure
was raised 24 millimeters with a corresponding increase of 90 per
cent in the muscular contraction; and in Fig. 15 C 30 millimeters
with a betterment of 125 per cent.
[Illustration: Figure 15.--During the periods indicated in the
time line the left splanchnic nerves were stimulated. The vessels
of the left adrenal gland were tied off.]
Comparison of Figs. 13, 14 and 15 reveals that the improvement
of contraction of fatigued muscle is much greater when the blood
pressure is raised, even slightly, from a low level, than when it
is raised, perhaps to a very marked degree, from a high level. In
one of the experiments performed by Nice and myself the arterial
pressure was increased by splanchnic stimulation from the low level
of 48 millimeters of mercury to 110 millimeters, and the height of
the muscular contractions was increased about sixfold (see Fig.
16).
[Illustration: Figure 16.--The bottom record (zero of blood
pressure) shows stimulation of left splanchnics; between the arrows
the pressure was kept from rising by compression of heart.]
Results confirming those described above were obtained by Gruber in a
study of the effects of splanchnic stimulation on the irritability of
muscle when fatigued. In a series of eleven observations the average
value of the barely effective stimulus (the “threshold” stimulus)
had to be increased as the condition of fatigue developed. It was
increased for the nerve-muscle by 25 per cent and for the muscle by
75 per cent. The left splanchnic nerves, disconnected from the left
adrenal gland, were now stimulated. The arterial pressure, which
had varied between 90 and 100 millimeters of mercury, was raised at
least 40 millimeters. As a result of splanchnic stimulation there
was an average recovery of 42 per cent in the nerve-muscle and of
46 per cent in the muscle. The increased general blood pressure
was effective, therefore, quite apart from any possible action of
adrenal secretion, in largely restoring to the fatigued structures
their normal irritability.
The Effect of Decreasing Arterial Pressure
Inasmuch as an increase in arterial pressure produces an increase
in the height of contraction of fatigued muscle, it is readily
supposable that a decrease in the pressure would have the opposite
effect. Such is the case only when the blood pressure falls below
the region of 90 to 100 millimeters of mercury. Thus if the arterial
pressure stands at 150 millimeters of mercury, it has to fall
approximately 55 to 65 millimeters before causing a decrease in
the height of contraction. Fig. 17 is the record of an experiment
in which the blood pressure was lowered by lessening the output of
blood from the heart by compressing the thorax. The record shows
that when the pressure was lowered from 120 to 100 millimeters of
mercury (A), there was no appreciable decrease in the height of
contraction; when lowered to 90 millimeters (B), there resulted a
decrease of 2.4 per cent; when to 80 millimeters of mercury (C), a
decrease of 7 per cent; and when to 70 millimeters (D), a decrease
of 17.3 per cent. Results similar to those represented in Fig. 17
were obtained by pulling on a string looped about the aorta just
above its iliac branches, thus lessening the flow to the hind limbs.
[Illustration: Figure 17.--The arrows indicate the points at which
the thorax began to be compressed in order to lessen the output of
blood from the heart.]
The region of 90 to 100 millimeters of mercury may therefore be
regarded as the _critical region_ at which a falling blood pressure
begins to be accompanied by a concurrent lessening of the efficiency
of muscular contraction, when the muscle is kept in continued
activity. It is at that region that the blood flow is dangerously
near to being inadequate.
An Explanation of the Effects of Varying the
Arterial Pressure
How are these effects of increasing and decreasing the arterial
blood pressure most reasonably explained? There is abundant evidence
that fatigue products accumulate in a muscle which is doing
work, and also that these metabolites interfere with efficient
contraction. As Ranke[82] long ago demonstrated, if a muscle,
deprived of circulating blood, is fatigued to a standstill, and
then the circulation is restored, the muscle again responds for a
short time to stimulation, because the waste has been neutralized
or swept away by the fresh blood. When the blood pressure is at
its normal height for warm-blooded animals (about 120 millimeters
of mercury, see Fig. 13), the flow appears to be adequate to wash
out the depressive metabolites, at least in the single muscle used
in these experiments, because a large rise of pressure produces
but little change in the fatigue level. On the other hand, when
the pressure is abnormally low, the flow is inadequate, and the
waste products are permitted to accumulate and clog the action of
the muscle. Under such circumstances a rise of pressure has a very
striking beneficial effect.
It is noteworthy that the best results of adrenin on fatigued
muscle reported by previous observers were obtained from studies on
cold-blooded animals. In these animals the circulation is maintained
normally by an arterial pressure about one-third that of warm-blooded
animals. Injection of adrenin in an amount which would not shut off
the blood supply would, by greatly raising the arterial pressure,
markedly increase the circulation of blood in the active muscle.
In short, the conditions in cold-blooded animals are quite like
those in the pithed mammal with an arterial pressure of about 50
millimeters of mercury (see Fig. 16). Under these conditions the
improved circulation causes a remarkable recovery from fatigue. That
notable results of adrenin on fatigue are observed in warm-blooded
animals only when they are deeply anesthetized or are deprived of
the medulla was claimed by Panella.[83] He apparently believed that
in normal mammalian conditions adrenin has little effect because
quickly destroyed, whereas in the cold-blooded animals, and in
mammals whose respiratory, circulatory, and thermogenic states are
made similar to the cold-blooded by anesthesia or pithing, the
contrary is true. In accordance with our observations of the effects
of blood pressure on fatigued muscle, we would explain Panella’s
results not as he has done but as due to two factors. First, the
efficiency of the muscle, when blood pressure is low, follows the
ups and downs of pressure much more directly than when the pressure
is high. And second, a given dose of adrenin always raises a low
blood pressure in atonic vessels. The improvement of circulation
is capable of explaining, therefore, the main results obtained in
cold-blooded animals and in pithed mammals.
Oliver and Schäfer reported unusually effective contractions in
muscles removed from the body after adrenal extract had been
injected. As shown in Fig. 16, however, the fact that the circulation
_had been_ improved results in continued greater efficiency of the
contracting muscle. Oliver and Schäfer’s observation may reasonably
be accounted for on this basis.
The Value of Increased Arterial Pressure in
Pain and Strong Emotion
As stated in a previous paragraph, there is evidence that the
vessels supplying a muscle dilate when the muscle becomes active.
And although the normal blood pressure (about 120 millimeters of
mercury) may be able to keep adequately supplied with blood the
single muscle used in our investigation, a higher pressure might
be required when more muscles are involved in activity, for a more
widely spread dilation might then reduce the pressure to the point
at which there would be insufficient circulation in active organs.
Furthermore, with many muscles active, the amount of waste would
be greatly augmented, and the need for abundant blood supply would
thereby to a like degree be increased. For both reasons a rise
of general arterial pressure would prove advantageous. The high
pressure developed in excitement and pain, therefore, might be
specially serviceable in the muscular activities which are likely
to accompany excitement and pain.
In connection with the foregoing considerations, the action
of adrenin on the distribution of blood in the body is highly
interesting. By measuring alterations in the volume of various
viscera and the limbs, Oliver and Schäfer[84] proved that the
viscera of the splanchnic area--e. g., the spleen, the kidneys,
and the intestines--suffer a considerable decrease of volume when
adrenin is administered, whereas the limbs into which the blood is
forced from the splanchnic region actually increase in size. The
action of adrenin indicates the relative degrees of sympathetic
innervations. In other words, at times of pain and excitement
sympathetic discharges, probably aided by the adrenal secretion
simultaneously liberated, will drive the blood out of the vegetative
organs of the interior, which serve the routine needs of the body,
into the skeletal muscles which have to meet by extra action the
urgent demands of struggle or escape.
But there are exceptions to the general statement that by adrenin
the viscera are emptied of their blood. It is well known that
adrenin has a vasodilator, not a vasoconstrictor, action on the
arteries of the heart; it is well known also that adrenin affects
the vessels of the brain and the lungs only slightly if at all.
From this evidence we may infer that sympathetic impulses, though
causing constriction of the arteries of the abdominal viscera, have
no effective influence on those of the pulmonary and intracranial
areas and actually increase the blood supply to the heart. Thus the
absolutely and immediately essential organs--those the ancients
called the “tripod of life”--the heart, the lungs, the brain (as
well as its instruments, the skeletal muscles)--are in times of
excitement abundantly supplied with blood taken from organs of less
importance in critical moments. This shifting of the blood so that
there is an assured adequate supply to structures essential for the
preservation of the individual may reasonably be interpreted as
a fact of prime biological significance. It will be placed in its
proper setting when the other evidence of bodily changes in pain
and excitement have been presented.
REFERENCES
[Footnote 80: McCurdy: American Journal of Physiology, 1901, v, p.
98.]
[Footnote 81: Kaufmann: Archives de Physiologie, 1892, xxiv, p.
283.]
[Footnote 82: Ranke: Archiv für Anatomie, 1863, p. 446.]
[Footnote 83: Panella: Archives Italiennes de Biologie, 1907,
xlviii, p. 462.]
[Footnote 84: Oliver and Schäfer: Journal of Physiology, 1895,
xviii, p. 240.]
CHAPTER VIII
THE SPECIFIC RÔLE OF ADRENIN IN COUNTERACTING THE
EFFECTS OF FATIGUE
As a muscle approaches its fatigue level, its contractions are
decreased in height. Higher contractions will again be elicited
if the stimulus is increased. Although these phenomena are well
known, no adequate analysis of their causes has been advanced. A
number of factors are probably operative in decreasing the height
of contraction: (1) The using up of available energy-producing
material; (2) the accumulation of metabolites in the fatigued muscle;
(3) polarization of the nerve at the point of repeated electrical
stimulation; and (4) a decrease of irritability. It may be that
there are interactions between these factors within the muscle, e.
g., the second may cause the fourth.
Variations of the Threshold Stimulus as a
Measure of Irritability
The last of the factors mentioned above--the effect of fatigue
on the irritability of the nerve-muscle combination, or on the
muscle alone--can be tested by determining variations in the least
stimulus capable of causing the slightest contraction, the so-called
“threshold stimulus.” As the irritability lessens, the threshold
stimulus must necessarily be higher. The height of the threshold is
therefore a measure of irritability. How does fatigue affect the
irritability of nerve-muscle and muscle? How is the irritability
of fatigued structures affected by rest? How is it influenced by
adrenin or by adrenal secretion? Answers to these questions were
sought in researches carried on by C. M. Gruber[85] in 1913.
The Method of Determining the Threshold Stimulus
The neuro-muscular arrangements used in these researches were in
many respects similar to those already described in the account
of experiments by Nice and myself. To avoid the influence of an
anesthetic some of the animals were decerebrated under ether and then
used as in the experiments in which urethane was the anesthetic. The
nerve (the _peroneus communis_) supplying the _tibialis anticus_
muscle was bared and severed; and near the cut end shielded platinum
electrodes were applied. These electrodes were used in fatiguing
the muscle. Between these electrodes and the muscle other platinum
electrodes could be quickly applied to determine the threshold
stimulus and the tissue resistance. These second electrodes were
removed except when in use, and when replaced were set always in
the same position. Care was taken, before replacing them, to wipe
off moisture on the nerve or on the platinum points.
For determining the threshold stimulus of the muscle the skin and
other overlying tissues were cut away from the _tibialis anticus_ in
two places about 5 centimeters apart. Through these openings platinum
needle electrodes could be thrust into the muscle whenever readings
were to be taken. Local polarization was avoided by reinserting
the needles into fresh points on the exposed areas whenever new
readings were to be taken.
The tendon of the _tibialis anticus_ was attached, as in the previous
experiments, by a strong thread passing about pulleys to a lever
which when lifted stretched a spring. During the determination of
the threshold the spring was detached from the lever, so that only
the pull of the lever itself (about 15 grams) was exerted on the
muscle.
The method of measuring the stimulating value of the electric current
which was used in testing the threshold was that devised by E. G.
Martin[*] of the Harvard Laboratory--a method by which the strength
of an induced electric shock is calculable in definite units.
If the tissue resistance enters into the calculation these are
called β units. When the threshold of the nerve-muscle was taken,
the apparatus for the determination was connected with the nerve
through the electrodes nearer the muscle. They were separated from
the fatiguing electrodes by more than 3 centimeters, and arranged
so that the kathode was next the muscle. When the threshold of
the muscle was taken directly the apparatus was connected with
the muscle through platinum needle electrodes thrust into it. The
position of the secondary coil of the inductorium, in every case,
was read by moving it away from the primary coil until the very
smallest possible contraction of the muscle was obtained. Four of
these readings were made, one with tissue resistance, the others
with 10,000, 20,000, and 30,000 ohms additional resistance in the
secondary circuit. Only break shocks were employed--the make shocks
were short-circuited. Immediately after the determination of the
position of the secondary coil, and before the electrodes were
removed or disconnected, three readings of the tissue resistance
were made. From these data four values for β were calculated.
*[Footnote: For a full account of Dr. Martin’s method of
calculating the strength of electric stimuli, see Martin: The
Measurement of Induction Shocks, New York, 1912.]
The strength of the primary current for determining the threshold
of the nerve-muscle was usually .01 ampere, but in a few cases
.05 ampere was used. For normal muscle it was .05 ampere and for
denervated muscle 1.0 ampere. The inductorium, which was used
throughout, had a secondary resistance of 1400 ohms. This was added
to the average tissue resistance in making corrections--corrections
were made also for core magnetization.
The Lessening of Neuro-muscular Irritability by Fatigue
The threshold for the _peroneus communis_ nerve in decerebrate
animals varied from 0.319 to 2.96 units, with an average in sixteen
experiments of 1.179.[*] This average is the same as that found by
E. L. Porter[86] for the radial nerve in the spinal cat. For animals
under urethane anesthesia a higher average was obtained. In these
it varied from .644 to 7.05, or an average in ten experiments of
3.081.
*[Footnote: For the detailed data of these and other quantitative
experiments, the reader should consult the tables in the original
papers.]
The threshold for the _tibialis anticus_ muscle varied in the
decerebrate animals from 6.75 units to 33.07, or an average in
fifteen experiments of 18.8. Ten experiments were performed under
urethane anesthesia and the threshold varied from 12.53 to 54.9,
with an average of 29.84 β units. From these results it is evident
that anesthesia notably affects the threshold.
E. L. Porter proved, by experiments carried on in the Harvard
Physiological Laboratory, that the threshold of an undisturbed
nerve-muscle remains constant for hours, and his observation was
confirmed by Gruber (see Fig. 19). If, therefore, after fatigue, a
change exists in the threshold, this change is necessarily the result
of alterations set up by the fatigue process in the nerve-muscle
or muscle.
After fatigue the threshold of the nerve-muscle, in sixteen
decerebrate animals, increased from an average of 1.179 to 3.34--an
increase of 183 per cent. In ten animals under urethane anesthesia
the threshold after fatigue increased from a normal average of 3.08
to 9.408--an increase of 208 per cent.
An equal increase in the threshold stimulus was obtained from the
normal muscle directly. In decerebrate animals the normal threshold
of 18.8 units was increased by fatigue to 69.54, or an increase
of 274 per cent. With urethane anesthesia the threshold increased
from 29.849 to 66.238, or an increase of 122 per cent.
Fig. 18, plotted from the data of one of the many experiments, shows
the relative heights of the threshold before and after fatigue. The
correspondence of the two readings of the threshold, one from the
nerve supplying the muscle and the other from the muscle directly,
served as a check on the electrodes. The broken line in the figure
represents the threshold (in units) of the nerve-muscle, and the
continuous line that of the muscle. The threshold values of the
nerve-muscle have been magnified ten times in order to bring the
two records close together. In this experiment the threshold of
the muscle after fatigue (i. e., at 2) is 167 per cent higher than
the normal threshold (at 1), while that of the nerve-muscle after
fatigue is 30.5 per cent higher than its normal.
[Illustration: Figure 18.--A record plotted from the data of one
experiment. The time intervals in minutes are registered on the
abscissa; the value of the threshold in units is registered on
the ordinate. The continuous line is the record of the muscle,
the broken line that of the nerve-muscle. The values for the
nerve-muscle have been magnified ten times, those for the muscle
are normal.
(1) Normal values of the threshold.
(2) Fatigue thresholds after one hour’s work, lifting 120 grams
240 times a minute.
(3 and 4) The threshold after rest.]
Evidently a direct relation exists between the duration of work and
the increase of threshold. For instance, the threshold is higher
after a muscle is fatigued for two hours than it is at the end of
the first hour. The relation between the work done and the threshold
is not so clear. In some animals the thresholds were higher after
120 grams had been lifted 120 times a minute for 30 minutes than
they were in others in which 200 grams had been lifted 240 times
a minute for the same period. The muscle in the latter instances
did almost four times as much work, yet the threshold was lower.
The difference may be due to the general condition of the animal.
A few experiments were performed on animals in which the nerve
supplying the muscle was cut seven to fourteen days previous to the
experiment. The muscle, therefore, had within it no living nerve
fibres. The average normal threshold for the denervated muscle in
6 animals was 61.28 units. As in the normal muscle, the percentage
increase due to fatigue was large.
The Slow Restoration of Fatigued Muscle to
Normal Irritability by Rest
That rest decreases the fatigue threshold of both nerve-muscle and
muscle can be seen in Fig. 18. The time taken for total recovery,
however, is dependent upon the amount of work done, but this change,
like that of fatigue, varies widely with different individuals. In
some animals the threshold returned to normal in 15 minutes; in
others, in which the same amount of work was done, it was still
above normal even after 2 hours of rest. This may be due to the
condition of the animals--in some the metabolites are probably
eliminated more rapidly than in others. There were also variations
in the rate of restoration of the normal threshold when tested on
the nerve and when tested on the muscle in the same animal. In
Fig. 18 (at 3) the nerve-muscle returned to normal in 30 minutes,
whereas the muscle (at 4) after an hour’s rest had not returned
to normal by a few β units. This, however, is not typical of all
nerve-muscles and muscles. The opposite condition--that in which
the muscle returned to normal before the nerve-muscle--occurred
in as many cases as did the condition just cited. The failure of
the two tissues to alter uniformly in the same direction may be
explained as due to variations in the location of the electrodes
when thrust into the muscle at different times (e. g., whether near
nerve filaments or not). The results from observations made on the
nerve are more likely to be uniform and reliable than are those
from the muscle.
The time required for the restoration of the threshold from fatigue
to normal, in denervated muscles, is approximately the same as that
for the normal muscle.
The Quick Restoration of Fatigued Muscle to
Normal Irritability by Adrenin
The foregoing observations showed that fatigue raises the normal
threshold of a muscle, on the average, between 100 and 200 per cent
(it may be increased more than 600 per cent); that this increase
is dependent on the time the muscle works, but also varies with
the animal; that rest, 15 minutes to 2 hours, restores the normal
irritability; and that this recovery of the threshold depends upon
the time given to rest, the duration of the work, and also upon
the condition of the animal. The problem which was next attacked
by Gruber was that of learning whether the higher contractions of
fatigued muscle after splanchnic stimulation could be attributed
to any influence which adrenal secretion might have in restoring
the normal irritability. To gain insight into the probabilities he
tried first the effects of injecting slowly into the jugular vein
physiological amounts of adrenin.[*]
*[Footnote: The form of adrenin used in these and in other
injections was fresh adrenalin made by Parke, Davis & Co.]
The normal threshold of the _peroneus communis_ nerve varied in the
animals used in this series of observations from 0.35 to 5.45 units,
with an average in nine experiments of 1.3, a figure close to the
1.179 found in the earlier series on the effect of fatigue. For the
_tibialis anticus_ muscle, in which the nerve-endings were intact,
the threshold varied from 6.75 to 49.3 units, with an average in
the nine experiments of 22.2. This is slightly higher than that
cited for this same muscle in the earlier series. By fatigue the
threshold of the nerve-muscle was increased from an average of 1.3
to an average of 3.3 units, an increase of 154 per cent. The muscle
increased from an average of 22.2 to an average of 59.6, an increase
of 169 per cent. After an injection of 0.1 to 0.5 cubic centimeters
of adrenin (1:100,000) the fatigue threshold was decreased _within
five minutes_ in the nerve-muscle from an average of 3.3 to 1.8,
a recovery of 75 per cent, and in the muscle from an average of
59.6 to 42.4, a recovery of 46 per cent. To prove that this effect
of adrenin is a _counteraction of the effects of fatigue_, Gruber
determined the threshold for muscle and nerve-muscle in non-fatigued
animals before and after adrenin injection. He found that in these
cases no lowering of threshold occurred, a result in marked contrast
with the pronounced and prompt lowering induced by this agent in
muscles when fatigued.
Figs. 19 and 20, plotted from the data of two of the experiments,
show the relative heights of the threshold before and after an
injection of adrenin. The close correspondence of the two readings
of the threshold, one from the nerve supplying the muscle, the other
from the muscle directly, served to show that there was no fault
in the electrodes. The continuous line in the Figures represents
the threshold (in units) of the muscle, the broken line that of the
nerve-muscle. The threshold of the nerve-muscle is magnified 100
times in Fig. 19 and 10 times in Fig. 20. In Fig. 19 (at 2 and 4)
the threshold was taken after an intravenous injection of 0.1 and
0.2 cubic centimeter of adrenin respectively.
These examples show that adrenin does not affect the threshold of
the normal non-fatigued muscle when tested either on the muscle
directly or on the nerve-muscle. In Fig. 19 (at 3) the observation
taken after two hours of rest illustrates the constancy of the
threshold under these circumstances.
In Fig. 19 the normal threshold was increased by fatigue (at 5)--the
muscle had been pulling 120 times a minute for one hour on a spring
having an initial tension of 120 grams--from 30.0 to 51.6 units,
an increase of 72 per cent; and in the nerve-muscle from 0.62 to
0.89 units, an increase of 46 per cent. The threshold (at 6) was
taken _five minutes_ after injecting 0.1 cubic centimeter of adrenin
(1:100,000). The threshold of the muscle was lowered from 51.6 to
38.0 units, a recovery of 62 per cent; that of the nerve-muscle
from 0.89 to 0.79 units, a recovery of 37 per cent. After another
injection of 0.5 cubic centimeter of adrenin the thresholds (at
7) were taken; that of the nerve-muscle dropped to normal--0.59
units--a recovery of 100 per cent, and that of the muscle remained
unaltered--26 per cent above its normal threshold.
[Illustration: Figure 19.--A record plotted from the data of
one experiment. The time intervals in hours and minutes are
represented on the abscissa; the values of the threshold in β
units are represented on the ordinate. The continuous line is the
record of the muscle, the broken line that of the nerve-muscle.
The nerve-muscle record is magnified 100 times; that of the muscle
is normal.
(1) Normal threshold stimulus. (2) Threshold five minutes after
an intravenous injection of 0.1 cubic centimeter of adrenin
(1:100,000) without previous fatigue. (3) Threshold after a rest
of two hours. (4) Threshold five minutes after an injection of 0.2
cubic centimeter of adrenin (1:100,000) without previous fatigue.
(5) Threshold after one hour’s fatigue. The muscle contracted
120 times per minute against a spring having an initial tension
of 120 grams. (6) Threshold five minutes after an injection (0.1
cubic centimeter) of adrenin (1:100,000). (7) Threshold five
minutes after another injection of adrenin (0.5 cubic centimeter
of a 1:100,000 solution).]
In Fig. 20 the threshold (at 5) was taken five minutes after an
injection of 0.1 cubic centimeter of adrenin. The drop here was as
large as that shown in Fig. 19. The threshold taken from the muscle
directly was lowered from 30.6 to 18 units, a recovery of 61 per
cent; the nerve-muscle from 1.08 to 0.87 units, a recovery of 51
per cent. That this sudden decrease cannot be due to rest is shown
in the same Figure (at 3 and 4). These readings were made after 60
and 90 minutes’ rest respectively. The sharp decline in the record
(at 5) indicates distinctly the remarkable restorative influence
of adrenin in promptly lowering the high fatigue threshold of
neuro-muscular irritability.
[Illustration: Figure 20.--A record plotted from the data of
one experiment. The time intervals in hours and minutes are
registered on the abscissa; the values of the threshold in units
are registered on the ordinate. The continuous line is the record
of the muscle, the broken line that of the nerve-muscle. The
record of the nerve-muscle is magnified ten times; that of the
muscle is normal.
(1) Normal threshold. (2) The threshold after one hour’s fatigue.
The muscle contracted 120 times per minute against a spring having
an initial tension of 120 grams. (3 and 4) Thresholds after rest;
after 60 minutes (3), and after 90 minutes (4). (5) Threshold
five minutes after an injection of adrenin (0.1 cubic centimeter
of a 1:100,000 solution). (6 and 7) Thresholds after rest; after
60 minutes (6), and after 90 minutes (7).]
The Evidence that the Restorative Action of
Adrenin is Specific
As stated in describing the effects of arterial blood pressure,
an increase of pressure is capable of causing a decided lowering
of the neuro-muscular threshold after fatigue. Is it not possible
that adrenin produces its beneficial effects by bettering the
circulation?
Nice and I had argued that the higher contractions of fatigued
muscle, that follow stimulation or injection of adrenin, could not
be wholly due to improved blood flow through the muscle, for when by
traction on the aorta or compression of the thorax arterial pressure
in the hind legs was prevented from rising, splanchnic stimulation
still caused a distinct improvement, the initial appearance of
which coincided with the point in the blood-pressure curve at which
evidence of adrenal secretion appeared. And, furthermore, the
improvement was seen also when adrenin was given intravenously in
such weak solution (1:100,000) as to produce a _fall_ instead of a
rise of arterial pressure. Lyman and I had shown that this fall of
pressure was due to a dilator effect of adrenin. Since the blood
vessels of the fatigued muscle were dilated by severance of their
nerves when the nerve trunk was cut, and, besides, as previously
stated (see p. 86), were being stimulated through their nerves at
a rate favorable to relaxation, it seemed hardly probable that
adrenin could produce its beneficial effect by further dilation
of the vessels and by consequent flushing of the muscle with an
extra supply of blood.[87] The lowering of blood pressure had
been proved to have no other effect than to impair the action of
the muscle (see p. 103). Although the chances were thus against an
interpretation of the beneficial influence of adrenin through action
on the circulation, it was thought desirable to test the possibility
by comparing its effect with that of another vasodilator--amyl
nitrite.
Figs. 21 and 22 are curves obtained from the left _tibialis anticus_
muscle. The rate of stimulation was 240 times a minute.
The muscle in Fig. 21 contracted against a spring having an initial
tension of 120 grams, and that in Fig. 22 against an initial tension
of 100 grams. In Fig. 21, at the point indicated on the base line,
0.4 cubic centimeter of adrenin (1:100,000) was injected into the
left external jugular vein. There resulted a fall of 25 millimeters
of mercury in the arterial pressure and a concurrent betterment of
15 per cent in the height of contraction, requiring two minutes
and fifteen seconds of fatigue (about 540 contractions) before it
returned to the former level. In Fig. 22, at the point indicated by
the arrow, a solution of amyl nitrite was injected into the right
external jugular vein. There resulted a fall of 70 millimeters of
mercury in arterial pressure and a betterment of 4.1 per cent in
the height of muscular contraction, requiring fifteen seconds of
fatigue (about 60 contractions) to decrease the height of contraction
to its former level. In neither case did the blood pressure fall
below the critical region (see p. 104).[*]
*[Footnote: In some cases after injection of amyl nitrite the
normal blood pressure, which was high, dropped sharply to a point
below the critical region. There resulted a primary increase in
muscular contraction due to the betterment in circulation caused
by the dilation of the vessels before the critical region was
reached. During the time that the pressure was below the critical
region the muscle contraction fell. As the blood pressure again
rose to normal the muscle contraction increased coincidently.]
[Illustration: Figure 21.--Top record, blood pressure with
mercury manometer. Middle record, contractions of the _tibialis
anticus_ muscle 240 times per minute against a spring with an
initial tension of 120 grams. Bottom record (zero blood pressure),
injection of 0.4 cubic centimeter of adrenin (1:100,000). Time
in half minutes.]
[Illustration: Figure 22.--Top record, blood pressure with mercury
manometer. Middle record, contractions of _tibialis anticus_
muscle 240 per minute against a spring with an initial tension
of 100 grams direct load. Bottom record (zero blood pressure),
time in half minutes. The arrow indicates the point at which a
solution of amyl nitrite was injected.]
Although the fall in arterial pressure caused by dilation of the
vessels due to amyl nitrite was almost three times as great as that
produced by the adrenin, yet the resultant betterment was only
about one-fourth the percentage height and lasted but one-ninth the
time. In all cases in which these solutions caused an _equal_ fall
in arterial pressure, adrenin caused higher contractions, whereas
amyl nitrite caused _no appreciable change_.
The Point of Action of Adrenin in Muscle
From the evidence presented in the foregoing pages it is clear that
adrenin somehow is able to bring about a rapid recovery of normal
irritability of muscle after the irritability has been much lessened
by fatigue, and that the higher contractions of a fatigued muscle
after an injection of adrenin are due, certainly in part, to some
specific action of this substance and not wholly to its influence
on the circulation. Some of the earlier investigators of adrenal
function, notably Albanese,[88] and also Abelous and Langlois,[89]
inferred from experiments on the removal of the glands that the
rôle they played in the bodily economy was that of neutralizing,
destroying or transforming toxic substances produced in the organism
as a result of muscular or nervous work. It seemed possible that
the metabolites might have a checking or blocking influence at the
junction of the nerve fibres with the muscle fibres, and might
thus, like curare, lessen the efficiency of the nerve impulses.
Radwánska’s observation[90] that the beneficial action of adrenin
is far greater when the muscle is stimulated through its nerve than
when stimulated directly, and Panella’s discovery[91] that adrenin
antagonizes the effect of curare, were favorable to the view that
adrenin improves the contraction of fatigued muscle by lessening
or removing a block established by accumulated metabolites.
The high threshold of fatigued denervated muscle, however, Gruber
found was quite as promptly lowered by adrenin as was that of normal
muscles stimulated through their nerves. Fig. 23 shows that the
height of contraction, also, of the fatigued muscle is increased
when adrenin is administered. In this experiment the left _tibialis
anticus_ muscle was stimulated directly by thrusting platinum
needle electrodes into it. The _peroneus communis_ nerve supplying
the muscle had been cut and two centimeters of it removed nine
days previous to the experiment. The rate of stimulation was 120
times per minute and the initial tension of the spring about 120
grams. At the point indicated by the arrow an injection of 0.1
cubic centimeter of adrenin (1:100,000) was made into a jugular
vein. A fall in arterial pressure from 110 to 86 millimeters of
mercury and a simultaneous betterment of 20 per cent in the height
of contraction were obtained. It required four minutes of fatigue
(about 480 contractions) to restore the muscle curve to its former
level. Results similar to this were obtained from animals in which
the nerve had been cut 7, 9, 12, 14, and 21 days. In all instances
the nerve was inexcitable to strong faradic stimulation.
[Illustration: Figure 23.--Top record, blood pressure with mercury
manometer. Middle record, contractions of a denervated muscle
(_tibialis anticus_) 240 per minute against a spring having an
initial tension of 120 grams (_peroneus communis_ nerve was cut
nine days before this record was taken). Bottom record (zero blood
pressure), time in half minutes. At the point indicated by an
arrow 0.1 cubic centimeter of adrenin (1:100,000) was injected
intravenously.]
In Radwánska’s experiments, mentioned above, the muscle was
stimulated directly when the nerve endings were intact. It seems
reasonable to suppose, therefore, that in all cases he was
stimulating nerve tissue. Since a muscle is more irritable when
stimulated through its nerve than when stimulated directly (nerve
and muscle), a slight change in the irritability of the muscle by
adrenin would naturally result in a greater contraction when the
nerve was stimulated. Panella’s results also are not inconsistent
with the interpretation that the effect of adrenin is on the muscle
substance rather than on the nerve endings. A method which has long
been used to separate muscle from nerve is that of blocking the
nervous impulses by the drug curare. Gruber found that when curare
is injected the threshold of the normal muscle is increased as was
to be expected from the removal of the highly efficient nervous
stimulations. And also, as was to be expected on that basis, curare
did not increase the threshold in a muscle in which the nerve endings
had degenerated. Adrenin antagonizes curare with great promptness,
decreasing the heightened threshold of a curarized muscle, in five
minutes or less, in some cases to normal. From this observation it
might be supposed that curare and fatigue had the same effect, and
that adrenin had the single action of opposing that effect. But
fatigue raises the threshold of a _curarized_ muscle, and adrenin
then antagonizes this fatigue. Langley[92] has argued that curare
acts upon a hypothetical “receptive substance” in muscle. If so,
probably curare acts upon a substance, or at a point, different from
that upon which fatigue acts; for, as the foregoing evidence shows,
fatigue increases the threshold of a muscle whether deprived of its
nerve supply by nerve section and degeneration or by curare, whereas
curare affects only the threshold of a muscle in which the nerve
endings are normal.[93] And since adrenin can oppose the effects
of both curare and fatigue, it may be said to have two actions, or
to act on two different substances or at two different points in
the muscle.
The evidence adduced in the last chapter indicated that the greater
“head” of arterial pressure produced by the more rapid heart beat
and the stronger contraction of many arterioles in times of great
excitement would be highly serviceable to the organism in any
extensive muscular activity which the excitement might involve. By
assuring an abundant flow of blood through the enlarged vessels
of the working muscle, the waste products resulting from the wear
and tear in contraction would be promptly swept away and thus would
be prevented from impairing the muscular efficiency. The adrenin
discharge at such times would, as was pointed out, probably reënforce
the effects of sympathetic impulses. The evidence presented in
this chapter shows that adrenin has also another action, a very
remarkable action, that of restoring to a muscle its original
ability to respond to stimulation, after that has been largely
lost by continued activity through a long period. What rest will
do only after an hour or more, adrenin will do in five minutes or
less. The bearing of this striking phenomenon on the functions of
the organism in times of great need for muscular activity will be
considered in a later discussion.
REFERENCES
[Footnote 85: Gruber: American Journal of Physiology, 1913, xxxii,
p. 437.]
[Footnote 86: E. L. Porter: American Journal of Physiology, 1912,
xxxi, p. 149.]
[Footnote 87: Cannon and Nice: American Journal of Physiology,
1913, xxxii, p. 55.]
[Footnote 88: Albanese: Archives Italiennes de Biologie, 1892,
xvii, p. 239.]
[Footnote 89: Abelous and Langlois: Archives de Physiologie, 1892,
xxiv, pp. 269-278, 465-476.]
[Footnote 90: Radwánska: Anzeiger der Akademie, Krakau, 1910, pp.
728-736. Reviewed in the Centralblatt für Biochemie und Biophysik,
1911, xi, p. 467.]
[Footnote 91: Panella: Archives Italiennes de Biologie, 1907, xlvii,
p. 30.]
[Footnote 92: Langley: Proceedings of the Royal Society of London,
1906, lxxviii, B, p. 181. Journal of Physiology, 1905-6, xxxiii,
pp. 374-413.]
[Footnote 93: See Gruber: American Journal of Physiology, 1914,
xxxiv, p. 89.]
CHAPTER IX
THE HASTENING OF COAGULATION OF BLOOD BY ADRENIN
The primary value of blood to the body must have been one of the
earliest observations of reasoning beings. When we consider the
variety of fundamental services which this circulating fluid
performs--the conveyance of food and oxygen to all the tissues,
the removal of waste, the delivery of the internal secretions,
the protection of the body against toxins and bacterial invasion,
and the distribution of heat from active to inactive regions--the
view of the ancient Hebrews that the “life of the flesh is in the
blood” is well justified. It is naturally of the utmost importance
that this precious fluid shall be safeguarded against loss. And its
property of turning to a jelly soon after escaping from its natural
channels assures a closure of the opening through which the escape
occurred, and thus protection of the body from further bleeding.
The slight evidence that adrenin hastens the clotting process has
already been hinted at. When we found that adrenin is set free in
pain and intense emotion, it seemed possible that there might exist
in the body an arrangement for making doubly sure the assurance
against loss of blood, a process that might nicely play its rôle
precisely when the greatest need for it would be likely to arise.
It was in 1903, while tracing in dogs the rise and fall of sugar
in the blood after administering adrenin, that Vosburgh and
Richards[94] first noted that simultaneously with the increase of
blood sugar there occurred more rapid coagulation. In some cases
the diminution was as much as four-fifths the coagulation time of
the control. Since this result was obtained by painting “adrenalin”
on the pancreas, as well as by injecting it into the abdominal
cavity, they concluded that “the phenomenon appears to be due to
the application of adrenalin to the pancreas.” Six years later,
during a study of the effect of adrenalin on internal hemorrhage,
Wiggers[95] examined incidentally the evidence presented by Vosburgh
and Richards, and after many tests on five dogs found “never the
slightest indication that adrenalin, either when injected or added
to the blood, appreciably hastened the coagulation process.” In 1911
von den Velden[3] reported that adrenin (about 0.007 milligram per
kilo of body weight) decreased the coagulation time in man about
one-half--an effect appearing 11 minutes after administration by
mouth, and 85 minutes after subcutaneous injection. He affirmed
also, but without describing the conditions or giving figures, that
adrenin decreases coagulation time _in vitro_. He did not attribute
the coagulative effect of adrenin in patients to this direct action
on the blood, however, but to vasoconstriction disturbing the normal
circulation and thereby the normal equilibrium between blood and
tissue. In consequence, the tissue juices with their coagulative
properties enter the blood, so he assumed. In support of this theory
he offered his observation that coagulation time is decreased after
the nasal mucosa has been rendered anemic by adrenin pledgets. Von
den Velden’s claim[96] for adrenin given by mouth was subjected to
a single test on man by Dale and Laidlaw,[97] but their result was
completely negative.
The importance of Vosburgh and Richards’ observation, the thoroughly
discordant testimony of later investigators, as well as the meager
and incidental nature of all the evidence that has been adduced
either for or against the acceleration of clotting by adrenin, made
desirable a further study of this matter. Especially was this further
study desirable because of the discharge of adrenin into the blood
in pain and emotional excitement. Accordingly, in 1914, H. Gray and
I[98] undertook an investigation of the question. In doing so we
employed cats as subjects. Usually they were quickly decerebrated
under ether, and then continuance of the drug became unnecessary.
Body temperature was maintained by means of an electric heating
pad. Respiration proceeded normally except in a few instances (in
which, presumably, there was hemorrhage into the medulla), when
artificial respiration had to be given.
The Graphic Method of Measuring the Coagulation Time
In order to avoid, so far as possible, the personal element in
determining when the blood was clotted, the blood was made to
record its own clotting. The instrument by means of which this
was done was the graphic coagulometer devised by W. L. Mendenhall
and myself,[99] and illustrated diagrammatically in Fig. 24. It
consists essentially of a light aluminum lever with the long arm
nearly counterpoised by a weight _W_. The long arm is prevented
from falling by a support _S_, and is prevented from rising by a
horizontal right-angled rod reaching over the lever at _R¹_ and
fixed into the block _B_ which turns on the axis _A_. Into the
same block is fixed the vertical rod _R²_. When this rod is moved
from the post _P¹_, against which it is held by the weight of the
horizontal rod _R¹_, towards the other post _P²_, the check on the
long arm of the lever is lifted, and if the short arm is heavier,
the long arm will then rise.
[Illustration: Figure 24.--Diagram of the graphic coagulometer.
The cannula at the right rests in a water bath not shown in this
diagram. For further description see text.]
The cannula _C_, into which the blood is received, is two centimeters
in total length and slightly more than two millimeters in internal
diameter. It is attached by a short piece of rubber tubing to the
tapered glass tube _T_, five centimeters long and five millimeters
in internal diameter. The upper end of this tube is surrounded by
another piece of rubber which supports the tube when it is slid
into the U-shaped support _U_, fixed directly below the end of the
short arm of the lever.
By drawing the cannulas from a single piece of glass tubing and
by making the distance from shoulder to upper end about twelve
millimeters, receptacles of fairly uniform capacity are assured.
All the dimensions, the reach of the rubber connection over the top
of the cannula (2-3 millimeters), the distance of the upper rubber
ring from the lower end of the glass chamber (4 centimeters), etc.,
were as nearly standard as possible.
A copper wire _D_, eight centimeters long and 0.6 millimeters in
diameter, bent above into a hook and below into a small ring slightly
less than two millimeters in diameter, is hung in a depression at
the end of the short arm of the lever. The small ring then rests
in the upper part of the cannula (see Fig. 24). The weight of the
copper wire makes the short arm of the lever heavier than the long
arm by 30 milligrams, when the delicate writing point is moving
over a lightly smoked drum. Half a dozen of these standard wires
are needed.
For accurate determination of the coagulation time Addis[100] has
defined the following conditions as essential:
1. The blood must always be obtained under the same conditions.
2. Estimates must all be made at the same temperature.
3. The blood must always come in contact with the same amount and
kind of foreign material.
4. The end point must be clear and definite and must always indicate
the same degree of coagulation.
The precautions taken to fulfill these conditions were as follows:
1. _Drawing the blood._--The blood was taken from the femoral
artery. The artery (usually the right) was laid bare in the groin
and freed from surrounding tissue. A narrow artery clip, with
each limb enclosed in soft rubber tubing (to prevent injury of
the tissues), and with its spring exerting gentle pressure, was
placed on the artery immediately below the deep femoral branch,
thus allowing no blood to stagnate above the clip. Between the clip
and a ligature applied about 1.5 centimeters below, an opening was
made. The blood was carefully milked out of the vessels between a
blunt dissector moved beneath, and a small forceps, twisted into
a pinch of absorbent cotton, moved above.
The cannula, cleaned in water, alcohol, and ether, was set in the
rubber connection of the glass tube; the point of the cannula was
then lubricated with vaseline and slipped into the artery. The
pressure of the clip on the artery was next very slightly released
and blood was allowed to flow into the cannula up to the lower
border of the rubber connection. Only a good-sized drop of blood
was needed. Sometimes the blood ran one or two millimeters above or
below, but without appreciably changing the result. Since the clip
was situated on the femoral immediately below a branch in which
the circulation persisted, _the blood received in the cannula was
always fresh from the moving stream_. As soon as the clip gripped the
artery again, the cannula was slipped out. A helper then promptly
milked the vessel in the manner described above, and covered it
with a pad of absorbent cotton smeared with vaseline to prevent
drying. Thereby blood was not permitted to stagnate; and when a new
sample was to be taken, the vessel was clean and ready for use.
The tip of the cannula was at once plugged by plunging it into a
flat mound of plasticine about three millimeters high. It was drawn
off sidewise lest the plasticine plug be pulled out again. One of
the copper wires _D_ was now slid into the tube and cannula, the
tube slipped into the U-support, and the wire lifted and hung on
the lever. This procedure, from the moment blood began to flow
until the wire was hung, consumed usually about twenty seconds.
2. _Uniform temperature._--Under the U-support was placed a large
water bath, in which the cannula and the tapering part of the tube
were submerged. A thermometer was fixed to the U-support so that
the bulb came near the cannula in the bath. The water was kept
within a degree of 25° C. This temperature was chosen for several
reasons: (a) The cannula has room temperature and rapidly cools the
small volume of blood that enters it. To heat blood and cannula to
body temperature would take time. A bath near room temperature,
therefore, seems preferable to one near body temperature. (b) The
test of clotting was conveniently made at intervals of a half-minute,
and if the clotting process were hastened by higher temperatures,
this interval would become relatively less exact. (c) A temperature
of 25° C. rather than lower was selected because, as Dale and
Laidlaw[101] have shown, the coagulation time is much slower for
a given change in temperature below 25° than for the same change
above. And with slowing of the process the end point, when the
determination depends on supporting a weight, is less likely to be
sharp. (d) The researches undertaken with use of this coagulometer
were concerned with factors hastening the process. For that reason
and for reason (b), a long rather than a short coagulation time
for normal conditions was desirable.
3. _Uniformity in the amount and kind of contact with foreign
surface._--The capacity of the cannulas was fairly uniform, as
stated above; the amount received in them was fairly constant; and
the wire hanging in the blood presented approximately the same
surface in different observations.
A further condition for insuring consistent treatment of the blood
in different cases was that of making the tests for coagulation
always at the same intervals. Below the writing point of the lever
was set an electromagnetic signal _E_, which recorded half-minutes.
At the moment a record was made by the signal (see first signal
mark, Fig. 25) the clip on the artery was opened, the blood taken,
and the process thus begun. In about 20 seconds the cannula was
suspended in the water bath and the wire was hanging on the lever.
At the next record by the signal and at every subsequent record the
vertical rod _R²_ was pushed with the index finger from post _P¹_
to post _P²_ and allowed to move back. This motion was uniform
and lasted about one second. The check _R¹_ on the long arm of
the lever was thus raised, and as the wire sank in the blood the
writing point rose, recording that coagulation had not taken place
(see Fig. 25).
[Illustration: Figure 25.--Record (reduced two-fifths) of five
successive tests of coagulation, with the animal in a uniform
condition. The lower line records intervals of 30 seconds. The
marks below the time record indicate the moments when the blood
samples were drawn.]
4. _Definite end point._--As soon as the blood clotted, the weight
of 30 milligrams was supported, and the failure of the lever to
rise to the former height in the regular time allowed, recorded
that the change had occurred.
Very rarely the swing of the lever would be checked for a moment
and would then begin to move rapidly, indicating that a strand
of fibrin had formed but not sufficiently strong to support the
weight, and that when the strand broke, the weight quickly sank in
the blood. If this occurred, the next record almost always was the
short line, which signified that the weight was well supported.
A very slight strand of fibrin was able to prevent the weight from
dropping, though at different times the amount of support differed,
as shown by the varying length of the final lines (compare first
and last series, Fig. 25). These variations are probably a rough
indication of the degree of coagulation. In our experiments, however,
the length of the final line was disregarded, and merely the fact
that the lever failed to swing through its usual distance was taken
as evidence of a clot, and the consequent short record was taken
as the end point.
As soon as this end point was registered, the tube, wire and cannula
were lifted out of the bath; the cannula was then separated from the
tube and pulled away from the wire. The clot was thus disclosed,
confirming the graphic record.
The method, at least when used at half-minute intervals, did not
reveal in all instances the same degree of clotting. Usually, when
the process was very rapid, the revealed clot was a thick jelly;
whereas, when the process was slow, a strand of fibrin or at most
a small amount of jelly was found. This difference in the _degree_
of coagulation introduced, of course, an element of inexactness.
In our experiments, however, this inexactness was unfavorable to
the result we were seeking for, i. e., the acceleration of the
process--because the jelly is a later stage than the fibrin strand;
and since we nevertheless obtained good evidence of acceleration, we
did not in these experiments attempt to determine more accurately
differences in the stage of the clotting process.
5. _Cleaning of apparatus._--After the wire was removed from the
tube, the clot attached to its ring-tip was carefully brushed away
under cool running water. Under the running water, also, a trimmed
feather was introduced into the cannula and the tube to push out the
plasticine and to wash out the blood. Wire, cannula and tube were
then dropped into a beaker receiving running hot water (about 80°
C.) and there allowed to remain for about five minutes. On removal
from this the parts were shaken free from water, passed through 95
per cent alcohol and again shaken free, passed through ether and
let dry.
By having a half-dozen cannulas and wires of standard size, it was
possible to save trouble by cleaning a number at one time.
Not infrequently the first few samples of blood taken from an animal
showed rapid or somewhat irregular rates of clotting. Some causes
for these initial variations will be presented in following pages.
The fairly uniform rate of clotting in any individual after the
initial stage, varied in twenty-one different animals from an average
of 3 to an average of 10.6 minutes, with a combined average of 5.9
minutes. The conditions for these variations among the individuals
have not been wholly determined.
The Effects of Subcutaneous Injections of Adrenin
The first observations were of this class.
Oct. 27. A cat weighing about 3 kilos was given 3 cubic centimeters
of adrenin 1:1,000, i. e., 1 milligram per kilo, under the skin. The
animal, in this instance, was kept in uniform ether anesthesia.
Following is a record showing when blood was taken, and the
coagulation time in each instance:
2.56--Injection made
.59--6 minutes
3.07--5.5 “
.13--5 “
.20--6.5 “
---
Average 5.7 minutes
3.27--3.5 minutes
.44--2 “
.55--2.5 “
4.07--3 “
.20--2 “
---
Average 2.6 minutes
4.44--6 minutes
5.00--4.5 “
5.50--5 “
---
Average 5.2 minutes
In this case the coagulation time remained at its usual level for
about 20 minutes after the subcutaneous injection.[*] Thereafter
for about an hour the coagulation time averaged 45 per cent of
its previous duration. And widely separated tests made during the
following hour indicated that approximately the initial rate of
clotting had been regained.
*[Footnote: This period is longer than is expected after the
subcutaneous injection of any drug. As will be shown later,
_strong_ doses of adrenin, if injected rapidly, may not at first
shorten the clotting process. Probably in some instances of
subcutaneous injection of these strong doses, the drug enters
the circulation more rapidly than in others and in consequence
coagulation is not at first accelerated.]
The rather long period (nearly 30 minutes), in the case just cited,
between the injection and the first appearance of rapid clotting was
not the rule. As the following figures show, the coagulation time
may become shortened quite promptly after subcutaneous injection.
Oct. 29. 3.30--5.5 minutes
.36--5.5 “
.44 Adrenin, 3 cubic centimeters, 1:1,000,
injected subcutaneously.
.46--5.5 minutes
.53--4 “
4.01--3.5 “
.08--3.5 “
.16--4.5 “
.23--5 “
.30--5.5 “
In this case nine minutes after the injection the change in the
rate of clotting had begun, and it continued more rapid for the
subsequent half-hour.
We did not attempt to find the minimal _subcutaneous_ dose which
would shorten clotting. A dose of 0.01 milligram per kilo, however,
has proved effective, as shown by the following figures:
Feb. 3. 11.34--10 minutes
.45-- 9 “
.50 to .52 Adrenin, 2.8 cubic centimeters, 1:100,000,
injected under skin of groin in cat weighing
2.8 kilos.
.55--10 minutes
12.06-- 7 “
.14-- 4 “
.19-- 5.5 “
.31-- 6 “
.37-- 7 “
.45-- 9 “
As will be shown later, the dose in this instance was ten times
the minimal effective _intravenous_ dose. On the basis of these
figures, less than a milligram of adrenin given subcutaneously
would be necessary to shorten clotting to a marked degree in a man
of average weight (70 kilograms).
Not many observations were made by us on the effects of adrenin
administered subcutaneously. The amount reaching the vascular
system and the rate of its entrance into the blood could be so much
more accurately controlled by intravenous than by subcutaneous
introduction that most of our attention was devoted to the latter
method.
The Effects of Intravenous Injections
In this procedure a glass cannula was fastened in one of the
external jugular veins and filled with the same solution as that to
be injected. A short rubber tube was attached and tightly clamped
close to the glass. Later, for the injection, the syringe needle
was inserted through the rubber and into the fluid in the cannula,
the clip on the vein was removed, and the injection made.
The solutions employed intravenously were adrenin 1:10,000, 1:50,000,
and 1:100,000, in distilled water.
The smallest amount which produced any change in clotting time was
0.1 cubic centimeter of a dilution of 1:100,000 in a cat weighing
two kilos, a dose of 0.0005 milligram per kilo. Four tests previous
to the injection averaged 5 minutes, and none was shorter than 4
minutes. Immediately after the injection the time was 2 minutes, but
at the next test the effect had disappeared. Doubling the dose in
the same cat--i. e., giving 0.2 cubic centimeter (0.001 milligram
per kilo)--shortened the coagulation time for about 40 minutes:
Dec. 23. 10.30--4 minutes
.35--4 “
.41--4 “
.46 Adrenin, 0.001 milligram per kilo.
.47--2.5 minutes
.50--3 “
.53--3.5 “
11.00--1.5 “
.05--1.5 “
.10--3 “
.15--2 “
.20--4 “
.26--4.5 “
.31--5 “
From 10.47, immediately after the second injection, till 11.20 the
average time for clotting was 2.5 minutes, whereas both before
and after this period the time was 4 minutes or longer. At 11.00
o’clock and 11.05, when the end point was reached in 1.5 minutes (a
reduction of 63 per cent), a thick jelly was found on examining the
cannula. The changes in clotting time in this case are represented
graphically in Fig. 26.
[Illustration: Figure 26.--Shortening of coagulation time after
injection of adrenin, 0.2 cubic centimeter, 1:100,000, (0.001
milligram per kilo), at 10:46. In this and following Figures a
scale for coagulation time is given in minutes at the left.]
In another case a dose of 0.0005 milligram per kilo failed to produce
any change, but 0.001 milligram per kilo (0.28 cubic centimeter
of adrenin, 1:100,000, given a cat weighing 2.8 kilos) brought a
sharp decline in the record, as follows:
Jan. 9. 11.32--6 minutes
.40--6 “
.47 Adrenin, 0.001 milligram per kilo.
.48--5.5 minutes
.55--4 “
12.00--5.5 “
.06--7 “
In these instances the animals were decerebrated. For decerebrate
cats, the least amount of adrenin, intravenously, needed to produce
shortening of coagulation time is approximately 0.001 milligram
per kilo.
In the above cases rapid clotting was manifest directly after
minute doses. Larger doses, however, may produce primarily not
faster clotting but slower, and that may be followed in turn by a
much shorter coagulation time. The figures below present such an
instance:
Nov. 25. 2.36--3 minutes
.40--3 “
.43 Adrenin, 0.5 cubic centimeter, 1:10,000.
.44--4 minutes
.49--3.5 “
.53--1.5 “
.55--1.5 “
.58--2 “
3.00--2.5 “
.03--1.5 “
.05--1.5 “
.07--2.5 “
.10--1.5 “
.14--1.5 “
.16--2.5 “
.19--3 “
.23--3 “
.30--3 “
This unexpected primary increase of coagulation time, lasting at
least six minutes, is in striking contrast to the later remarkable
shortening of the process from 3 to an average of 1.7 minutes for
more than 20 minutes (see Fig. 27, A).
[Illustration: Figure 27.--A, Primary lengthening followed by
shortening of the coagulation time when adrenin, 0.5 cubic
centimeter 1:10,000 (0.05 milligram), was injected slowly at 2:43.
B, Lengthening of the coagulation time without shortening when the
same dose was injected rapidly at 10:08.]
If a strong solution, i. e., 1:10,000, is injected rapidly, the
process may be prolonged as above, but not followed as above by
shortening, thus:
Nov. 28. 9.59--3 minutes
10.03--3 “
.08 Adrenin, 0.5 cubic centimeter, 1:10,000.
.10--3 minutes
.14--3.5 “
.18--3.5 “
.22--3.5 “
.26--3 “
.29--3 “
.33--3 “
There was in this case no decrease in coagulation time at any test
for a half-hour after the injection, but instead a lengthening (see
Fig. 27, B). Howell[102] has reported the interesting observation
that repeated massive doses of adrenin given to dogs may so greatly
retard coagulation that the animals may be said to be hemophilic.
These two instances show that on coagulation large doses have the
contrary effect to small, just as Hoskins[103] showed was true for
intestinal and Lyman and I[104] showed was true for arterial smooth
muscle.
In a few experiments the brain and the cord to midthorax were
destroyed through the orbit. Artificial respiration then maintained
the animal in uniform condition. Under these circumstances, adrenin
intravenously had more lasting effects than when given to the usual
decerebrate animals with intact cord. Fig. 28 illustrates such a
case. For thirty minutes before injection the clotting time averaged
5.4 minutes. Then, about ten minutes after one cubic centimeter
of adrenin, 1:50,000, had been slowly injected, clotting began
to quicken; during the next twenty minutes the average was 3.4
minutes, and during the following forty-five minutes the average
was 1.9 minutes--only 35 per cent as long as it had been before
the injection.
[Illustration: Figure 28.--Persistent shortening of the coagulation
time after injecting (in an animal with brain and upper cord
pithed) adrenin, 1 cubic centimeter, 1:50,000 (0.02 milligram),
at 11:01-02. The dash lines represent averages.]
In another case in which the brain and upper cord were similarly
destroyed, the clotting time, which for a half-hour had averaged 3.9
minutes, was reduced by one cubic centimeter of adrenin, 1:100,000,
to an average for the next hour and forty minutes of 2.3 minutes,
with 1.5 and 3 minutes as extremes. During the first forty minutes
of this period of one hour and forty minutes of rapid clotting all
of eight tests except two showed a coagulation time of 2 minutes or
less. The explanation of this persistent rapid clotting in animals
with spinal cord pithed is not yet clear.
As indicated in Figs. 26, 27 and 28, the records of coagulation show
oscillations. Some of these ups and downs are, of course, within
the limits of error of the method, but in our experience they have
occurred so characteristically after injection of adrenin, and so
often have appeared in a rough rhythm, that they have given the
impression of being real accompaniments of faster clotting. It
may be that two factors are operating, one tending to hasten, the
other to retard the process, and that the equilibrium disturbed by
adrenin is recovered only after interaction to and fro between the
two factors.
The oscillations in coagulation time after the injections suggest
that clotting might vary with changes in blood pressure, for that
also commonly oscillates after a dose of adrenin (see, e. g., Fig.
23). Simultaneous recording of blood pressure and determining
of coagulation time have revealed that each may vary without
corresponding variation in the other. Within ordinary limits,
therefore, changes of blood pressure do not change the rate of
clotting.
The Hastening of Coagulation by Adrenin Not a
Direct Effect on the Blood
As previously stated, von den Velden has contended that shortening
of coagulation time by adrenin is due to exudation of tissue juices
resulting from vasoconstriction. The amount of adrenin which
produces markedly faster clotting in the cat, is approximately 0.001
milligram per kilo. As Lyman and I[105] showed, however, this amount
when injected slowly, as in the present experiments, results in
brief vasodilation rather than vasoconstriction. Von den Velden’s
explanation can therefore not be applied to these experiments.
He has claimed, furthermore, that adrenin added to blood _in vitro_
makes it clot more rapidly, but, as already noted, he gives no
account of the conditions of his experiments and no figures. It is
impossible, therefore, to criticise them. His claim, however, is
contrary to Wiggers’s[106] earlier observations that blood with added
adrenin coagulated no more quickly than blood with an equal amount
of added physiological salt solution. Also contrary to this claim
are the following two experiments: (1) Ligatures were tied around
the aorta and inferior vena cava immediately above the diaphragm,
and thus the circulation was confined almost completely to the
anterior part of the animal. Indeed, since the posterior part ceases
to function in the absence of blood supply, the preparation may be
called an “anterior animal.” When such a preparation was made and
0.5 cubic centimeter of adrenin, 1:100,000 (half the usual dose,
because, roughly, half an animal), was injected slowly into one of
the jugulars, coagulation was not shortened. Whereas for a half-hour
before the injection the clotting time averaged 4.6 minutes, for an
hour thereafter the average was 5.3 minutes--a prolongation which
may have been due, not to any influence of adrenin, but to failure
of the blood to circulate through the intestines and liver.[107]
In another experiment after the gastro-intestinal canal and liver
had been removed from the animal, the average time for coagulation
during twenty-five minutes before injecting adrenin (0.23 cubic
centimeter, 1:100,000, in an animal weighing originally 2.3 kilos)
was 5.5 minutes, and during forty minutes after the injection it was
6.8 minutes, with no case shorter than 6 minutes. In the absence
of circulation through the abdominal viscera, therefore, adrenin
fails to shorten the clotting time. (2) The cannulas were filled
with adrenin, 1:1,000, and emptied just before being introduced into
the artery. The small amount of adrenin left on the walls was thus
automatically mixed with the drawn blood. Alternate observations
with these cannulas wet by adrenin and with the usual dry cannulas
showed no noteworthy distinction.
Feb. 19. 2.21--6 minutes, with usual cannula
.30--6.5 “ “ “ “
.36--6.5 “ “ adrenin “
.49--6 “ “ “ “
.56--7 “ “ usual “
3.04--6 “ “ adrenin “
The results of these experiments have made it impossible for us to
concede either of von den Velden’s claims, i. e., that clotting
occurs faster because adrenin is added to the blood, or because
adrenin by producing vasoconstriction causes tissues to exude
coagulant juices.
Vosburgh and Richards found that coagulation became more rapid
as the blood sugar increased. Conceivably faster clotting might
result from this higher percentage of blood sugar. Against this
assumption, however, is the fact that clotting is greatly accelerated
by 0.001 milligram adrenin per kilo of body weight, much less than
the dose necessary to increase the sugar content of the blood.[108]
And furthermore, when dextrose (3 cubic centimeters of a 10 per
cent solution) is added to the blood of an anterior animal, making
the blood sugar roughly 0.3 per cent, the coagulation time is not
markedly reduced. Adrenin appears to act, therefore, in some other
way than by increasing blood sugar.
Since adrenin makes the blood clot much faster than normally in the
intact animal, and fails to have this effect when the circulation
is confined to the anterior animal, the inference is justified that
in the small doses here employed adrenin produces its remarkable
effects, not directly on the blood itself, not through change in
the extensive neuro-muscular, bony, or surface tissues of the body,
but through some organ in the abdomen.
That exclusion of the liver from the bodily economy, by ligature
of its vessels or by phosphorus poisoning, will result in great
lengthening of the coagulation time has been clearly shown. The
liver, therefore, seems to furnish continuously to the blood a factor
in the clotting process which is being continuously destroyed in
the body. It is not unlikely that adrenin makes the blood clot
more rapidly by stimulating the liver to discharge this factor in
greater abundance. But proof for this suggestion has not yet been
established.
REFERENCES
[Footnote 94: Vosburgh and Richards: American Journal of Physiology,
1903, ix, p. 39.]
[Footnote 95: Wiggers: Archives of Internal Medicine, 1909, iii,
p. 152.]
[Footnote 96: Von den Velden: Münchener medizinische Wochenschrift,
1911, lviii, p. 187.]
[Footnote 97: Dale and Laidlaw: Journal of Pathology and
Bacteriology, 1912, xvi, p. 362.]
[Footnote 98: Cannon and Gray: American Journal of Physiology,
1914, xxxiv, p. 321.]
[Footnote 99: Cannon and Mendenhall: American Journal of Physiology,
1914, xxxiv, p. 225.]
[Footnote 100: Addis: Quarterly Journal of Experimental Physiology,
1908, i, p. 314.]
[Footnote 101: Dale and Laidlaw: _Loc. cit._, p. 359.]
[Footnote 102: Howell: American Journal of Physiology, 1914, xxxiii,
p. xiv.]
[Footnote 103: Hoskins: American Journal of Physiology, 1912, xxix,
p. 365.]
[Footnote 104: Cannon and Lyman: American Journal of Physiology,
1913, xxxi, p. 376.]
[Footnote 105: Cannon and Lyman: _Loc. cit._, p. 381.]
[Footnote 106: Wiggers: _Loc. cit._, p. 152.]
[Footnote 107: See Pawlow: Archiv für Physiologie, 1887, p. 458.
Bohr: Centralblatt für Physiologie, 1888, ii, p. 263. Meek: American
Journal of Physiology, 1912, xxx, p. 173. Gray and Lunt: _Ibid._,
1914, xxxiv, p. 332.]
[Footnote 108: Cannon: American Journal of Physiology, 1914, xxxiii,
p. 396.]
CHAPTER X
THE HASTENING OF THE COAGULATION OF BLOOD IN
PAIN AND GREAT EMOTION
In the foregoing chapter evidence was presented that the intravenous
injection of minute amounts of adrenin hastens the clotting of
blood. The amounts used did not vary much above or below the amounts
discharged by the adrenal glands after brief stimulation of the
splanchnic nerves, as found by H. Osgood in the Harvard Laboratory,
and may therefore be regarded as physiological. Since injected
adrenin is capable of shortening the coagulation time, may not the
increased secretion of the adrenals likewise have that effect? The
answer to this question was the object of an investigation by W.
L. Mendenhall and myself.[109]
The blood was taken and its coagulation was recorded graphically
in the manner already described. In some instances the cats were
etherized, in others they were anesthetized with urethane, or were
decerebrated. The splanchnic nerves always were stimulated after
being cut away from connection with the spinal cord. Sometimes
the nerves were isolated unilaterally in the abdomen; sometimes,
in order to avoid manipulation of the abdominal viscera, they
were isolated in the thorax and stimulated singly or together. A
tetanizing current was used, barely perceptible on the tongue and
too weak to cause by spreading any contraction of skeletal muscles.
Coagulation Hastened by Splanchnic Stimulation
That splanchnic stimulation accelerates the clotting of blood, and
that the effects vary in different animals, are facts illustrated
in the following cases:
Oct. 25.--A cat was etherized and maintained in uniform ether
anesthesia. After forty minutes of preliminary observation the left
splanchnic nerves were stimulated in the abdomen. Following are
the figures which show the effects on the coagulation time:
3.00--4 minutes
.07--5.5 “
.14--4 “
.32--4.5 “
.39 to .40 Stimulation of left splanchnic.
.42--5 minutes
.49--5 “
.56--2 “
4.00--1 “
.03--2.5 “
.07--2.5 “
.11--3 “
.16--2 “
.20--1.5 “
.23--4 “
.29--5.5 “
.40--5.5 “
.50--5 “
In this instance at least ten minutes elapsed between the end of
stimulation and the beginning of faster clotting. The period of
faster clotting, however, lasted for about a half-hour, during
which the coagulation time averaged 2.1 minutes, only forty-three
per cent of the previous average of 4.8 minutes. It is noteworthy
that the curve (see Fig. 29), while lower, shows oscillations not
unlike those which follow injection of adrenin (see p. 155).
[Illustration: Figure 29.--Shortening of coagulation time after
stimulation of the left splanchnic nerves, 3:39-:40.]
The primary delay of the effect is not always, indeed it is not
commonly, present:
Nov. 6.--A cat was anesthetized (1.40 p.m.) with urethane, and later
(3.05) its brain was pithed. The following observations on the
coagulation time show the prompt effect of splanchnic stimulation:
3.36--7 minutes
.46--6 “
4.02 to .05 Stimulation of left splanchnic in abdomen.
.08--4 minutes
.10--3 “
.18--3.5 “
.23--6.5 “
In Fig. 30 is presented the original record of the shortening of
the coagulation after stimulation of the left splanchnic nerve
(Nov. 8) in a cat with brain pithed.
[Illustration: Figure 30.--About one-third original size. Record
of shortening of coagulation time after stimulation of the left
splanchnic nerves, 4:33-:35. The time before stimulation was 6
minutes, and afterwards, 3, 4, 4, 4.5, and 6 minutes.]
In the foregoing instances the coagulation time was reduced after
splanchnic stimulation to less than half what it was before. The
reduction was not always so pronounced.
Nov. 7.--A cat[*] maintained in uniform ether anesthesia with
artificial respiration had the following changes in the clotting
time of its blood as the result of stimulating the left splanchnic
nerve in the thorax:
3.40--5 minutes
.45--5 “
.51--5.5 “
.58 to 4.00 Stimulation of left splanchnic.
4.01--4.5 minutes
.06--3.5 “
.11--4 “
.16--3.5 “
.21--4 “
.26--4.5 “
.31--5 “
.36--6.5 “
*[Footnote: This animal had just passed through a period of
excitement with rapid clotting.]
In this case the average for about fifteen minutes before stimulation
was slightly over five minutes, and for twenty-five minutes
thereafter it was four minutes.
In all cases thus far the period of shortened coagulation lasted
from ten to thirty minutes. In other cases, however, the effect was
seen only in a single observation. If this had occurred only once
after splanchnic stimulation, it might be attributed to accident,
but it was not an infrequent result, e. g.:
Oct. 28.--A cat was etherized and decerebrated, and the splanchnic
nerves were isolated in the thorax. Following are two instances of
brief shortening of coagulation after splanchnic stimulation:
3.36--4.5 minutes
.42--4.5 “
.47 to .49 Splanchnic stimulation.
.51--4.5 minutes
.57--2 “
4.01--4 “
.07--4.5 “
.12--5.5 “
.19 to .22 Splanchnic stimulation.
.23--3.5 minutes
.27--4 “
.33--5 “
In the foregoing instance it is noteworthy that the degree of
acceleration is not so great after the second stimulation of the
splanchnics as it was after the first. This reduction of effect as
the nerves were repeatedly stimulated was frequently noted. The
following case presents another illustration:
Nov. 12.--A cat was etherized (2.35 p.m.) and the medulla was
punctured (piqûre) at 3.12. The operation was without effect. The
loss or lessening of effectiveness on second stimulation of the
left splanchnic nerves is to be compared with the persistence of
effectiveness on the right side:
3.40--4.5 minutes
.45--4.5 “
.54 to .56 Stimulation of left splanchnic in abdomen.
4.00--3 minutes
.05--2 “
.10--5.5 “
.16--5 “
.22 to .27 Stimulation of left splanchnic in abdomen.
.30--4 minutes
.34--4 “
.39--4 “
.44--4 “
.48--4 “
.55 to .57 Stimulation of right splanchnic.
.59--3 minutes
5.02--2.5 “
.07--3 “
.11--3 “
.15--5.5 “
.22--5.5 “
The experiments above recorded show that stimulation of the
splanchnic nerves results immediately, or after a brief period,
in a shortening of the coagulation time of the blood--an effect
which in different animals varies in duration and intensity, and
diminishes as the stimulation is repeated. The next question was
whether this effect is produced through the adrenal glands.
Coagulation Not Hastened by Splanchnic Stimulation
if the Adrenal Glands are Absent
The manner in which splanchnic stimulation produces its effects is
indicated in the following experiments:
Nov. 28.--A cat was etherized, and through the orbit the central
nervous system was destroyed to the midthorax. The blood vessels
of the _left_ adrenal gland were then quickly tied and the gland
removed. The readings for a half hour before the left splanchnic
nerve was stimulated averaged seven minutes, then--
4.38 to .40 Stimulation of left splanchnic (glandless).
.42--7 minutes
.50--7 “
5.02 to .04 Stimulation of right splanchnic.
.06--4 minutes
.10--7 “
.18--7 “
.26--7 “
Dec. 4.--A cat was etherized and pithed through the orbit to the
neck region. The right and left splanchnic nerves were tied and cut
in the thorax. The _left_ adrenal gland was then carefully removed.
These operations consumed about a half-hour. The following records
show the effect of stimulating the left and right splanchnic nerves:
4.10--5 minutes
.16--4.5 “
.25 to .28 Stimulation of left splanchnic (glandless).
.30--4.5 minutes
.35--4.5 “
.40--7.5 “
.49 to .51 Stimulation of right splanchnic.
.55--4.5 minutes
5.00--2.5 “
.14--6 “
.23 to .25 Stimulation of right splanchnic.
.26--6 minutes
.33--4.5 “
.38--3.5 “
.43--4.5 “
.49--5 “
.55--6 “
The results in this experiment are represented graphically in Fig.
31.
[Illustration: Figure 31.--Results of stimulating the left
splanchnic nerves, 4:25-:28, after removal of the left adrenal
gland; and of stimulating the right splanchnic nerves, 4:49-:51
and 5:23-:25, with right adrenal gland present.]
Elliott’s evidence that in the cat the splanchnic innervation of the
adrenals is not crossed has already been mentioned. If the gland
is removed on one side, therefore, stimulation of the nerves on
that side causes no discharge from the opposite gland. As the above
experiments clearly show, splanchnic stimulation on the glandless
side results in no shortening of the coagulation time; whereas,
in the same animals, stimulation of the nerves on the other side
(still connected with the adrenal gland) produces a sharp hastening
of the clotting process.
The splanchnics innervate the intestines and liver even though the
adrenal gland is removed. The foregoing experiments indicate that
the nerve impulses delivered to these organs do not influence them
in any direct manner to accelerate the speed of coagulation. Indeed,
in one of the experiments (Dec. 4, see Fig. 31) a high reading about
ten minutes after splanchnic stimulation on the glandless side
suggests the possibility of an opposite effect. Direct stimulation
of the hepatic nerves on one occasion was followed by a change of
the clotting time from 4.5, 5, 4.5, 4.5 minutes during twenty-five
minutes before stimulation to 4.5, 7, and 6 minutes during twenty
minutes after stimulation.
Since with the adrenals present stimulation of hepatic nerves
induces alteration of glycogen in the liver and quick increase of
blood sugar,[110] just as splanchnic stimulation does, the failure
of the blood to clot faster after stimulation of the hepatic nerves
confirms the evidence already offered that faster clotting when
adrenin is increased in the blood is not due to a larger amount of
sugar present (see p. 159).
The liver and intestines cannot be made to shorten clotting time by
stimulation of their nerves, but, as has already been shown (see
p. 157), neither can adrenin act by itself to hasten the clotting
process. Apparently the effect is produced by coöperation between
the adrenals and the liver (and possibly also the intestines).
Somewhat similar coöperation is noted in the organization of sugar
metabolism; splanchnic stimulation in the absence of the adrenal
glands does not increase blood sugar,[111] and in the absence of
the liver adrenin is without influence.[112]
The variations of effect noted after splanchnic stimulation can be
accounted for by variations in the adrenin content of the glands.
Elliott[113] found, as previously stated, that animals newly brought
into strange surroundings may have a considerably reduced amount
of adrenin in their adrenals. The animals used in our experiments
had been for varying lengths of time in an animal house in which
barking dogs were also kept, and were therefore subject to influences
which would be likely to discharge the glands.
The evidence that stimulation of splanchnic nerves, with accompanying
increase of adrenal secretion, results in more rapid clotting of
blood is especially interesting in relation to the experiments
previously described, which showed that in pain and emotional
excitement there is an increased secretion of adrenin into the
blood. Does the adrenin thus liberated have any effect on the rate
of coagulation? The observations here recorded were made in order
to obtain an answer to that question.
Coagulation Hastened by “Painful” Stimulation
In the experiments on the action of stimuli which in the
unanesthetized animal would cause pain, it will be recalled that
faradic stimulation of a large nerve trunk (the stump of the cut
sciatic) and operation under light anesthesia were the methods used
to affect the afferent nerves. Elliott[114] found that repeated
excitation of the sciatic nerve was especially efficient in
exhausting the adrenal glands of their adrenin content, and also
that this reflex persisted after removal of the cerebral hemispheres.
It was to be expected, therefore, that with well-stored glands,
sciatic stimulation, even in the decerebrate animal, would call
forth an amount of adrenal secretion which would decidedly hasten
clotting. The following case illustrates such a result:
Dec. 12.--A cat was anesthetized with ether at 3.45 and the left
sciatic nerve was bared. Decerebration was completed at 3.57. The
clotting time of the blood began to be tested six minutes later:
4.03--4 minutes
.08--3.5 “
.13--3.5 “
.18--4.5 “
.23 to .25 Stimulation of left sciatic.
4.26--2.5 minutes
.29--3.5 “
.34--4 “
.40--5 “
.45 to .50 Stimulation of left sciatic.
4.53--2.5 minutes
.57--7 “
5.06--7.5 “
.15 to .17 Stimulation of left sciatic.
5.17--4 minutes
.22--4.5 “
.27--5.5 “
.36--5.5 “
.46--7 “
The results obtained in this case, which were similar to results in
other cases, are represented graphically in Fig. 32. The coagulation
time was becoming gradually more prolonged, but each excitation
of the sciatic nerve was followed by a marked shortening. The
strength of stimulation was not determined with exactness, but it
is worthy of note that the current used in the first and the third
stimulations was weaker than could be felt on the tongue, whereas
that used in the second was considerably stronger, though it did
not produce reflex spasms.
[Illustration: Figure 32.--Three shortenings of coagulation time
after stimulation of the left sciatic nerve, at 4:23-:25, at
4:45-:50 (stronger), and at 5:15-:17.]
Mere tying of the nerve is capable of producing a marked shortening
of coagulation, as the following figures show:
Oct. 21.--10.57 cat under ether, and urethane given:
11.11--8.5 minutes
.23--8.5 “
.32 to .35 Left sciatic bared and tied.
.37--1.5 minutes
.41--5.5 “
.50--7 “
12.02--8.5 “
Stimulation of the crural nerve had similar effects, reducing the
clotting time in one instance from a succession of 3, 3, and 3.5
minutes to 1.5 minutes shortly after the application of the current,
with a return to 3.5 minutes at the next test.
Operative procedures performed under light anesthesia (i. e.,
with the more persistent reflexes still present), or reduction of
anesthesia soon after operation, resulted in a remarkable shortening
of the coagulation time:
Nov. 8.--A cat was etherized and tracheotomized. The abdomen was
then opened and a ligature was drawn around the hepatic nerves. The
operation was completed at 2.25. At 2.50 the etherization became
light and the rate of clotting began to be faster:
2.50--6 minutes
3.00--5.5 “
.10--3.5 “
.15--3.5 “
.20--4.5 “
.30--7.5 “
Nov. 11.--A female cat, very quiet, was placed in the holder at
1.55. The animal was not excited. At 2.10 etherization was begun;
the animal was then tracheotomized, and the femoral artery was
exposed.
2.21--4.5 minutes
.26--4.5 “ Anesthesia lessened.
.32--3.5 “ “ light.
.35 Abdomen opened.
.47--1.5 minutes.
.52--1 “
.55 Ligature passed around hepatic nerves.
.57--1.5 minutes. Anesthesia light; corneal reflex present.
3.02--3 “
.07--3 “ Some hepatic nerves cut.
.12--4.5 “ Rest of hepatic nerves cut.
.22--5 “
The results of this experiment are shown graphically in Fig. 33.
[Illustration: Figure 33.--Shortening of coagulation time during an
operation under light anesthesia. At 2:35 the abdomen was opened,
at 2:55 a ligature was passed around the hepatic nerves.]
Nov. 13.--A cat was etherized at 1.55, tracheotomized, and the
femoral artery laid bare. As soon as these preparations were
completed, the ether was removed and anesthesia became light. The
blood clotted thus:
2.08--6 minutes
.15--4 “ Anesthesia light.
.20--2 “
.24--1 “ Etherization begun again.
.27--2.5 “
.30--3.5 “
.35--5.5 “
.50--5.5 “
In the foregoing and in other similar instances, a condition of
surgical injury, whether just made or being made, was accompanied
by more rapid clotting of blood when the degree of anesthesia was
lessened. This condition was one which, if allowed to go further in
the same direction, would result in pain. Both direct electrical
stimulation and also surgical operation of a nature to give pain in
the unanesthetized animal result, therefore, in faster clotting.
It is worthy of note that after decerebration clotting apparently
occurred no faster because the abdomen had been opened, although
in the decerebrate state etherization was suspended. The mechanism
for reflex control of the adrenals may not be higher than the
corpora quadrigemina, as Elliott has shown, but the discharge from
the glands seems to be more certain to occur when the cerebrum is
present and is permitted even slightly to operate.
Coagulation Hastened in Emotional Excitement
The evidence for emotional secretion of the adrenal glands has
already been presented. As was noted in my earlier observations on
the motions of the alimentary canal (see p. 14), cats differ widely
in their emotional reaction to being bound; some, especially young
males, become furious; others, especially elderly females, take the
experience quite calmly. This difference of attitude was used with
positive results, the reader will recall, in the experiments on
emotional glycosuria; there seemed a possibility likewise of using
it to test the effect of emotions on blood clotting. To plan formal
experiments for that purpose was not necessary, because in the
ordinary course of the researches here reported, the difference in
effects on the blood between the violent rage of vigorous young males
and the quiet complacency of old females was early noted. Indeed,
the rapid clotting which accompanied excitement not infrequently
made necessary an annoying wait till slower clotting would permit
the use of experimental methods for shortening the process.
The animals used on November 11 and 13 (see pp. 175, 176) are
examples of calm acceptance of being placed on the holder;
and furthermore, these animals were anesthetized without much
disturbance. As the figures indicate, the clotting from the first
occurred at about the average rate.
In sharp contrast to these figures are those obtained when a vigorous
animal is angered:
Oct. 30.--A very vigorous cat was placed on the holder at 9.08.
It at once became stormy, snarling, hissing, biting, and lashing
its big tail. At 9.12 etherizing was begun and that intensified
the excitement. By 9.15 the femoral artery was tied. The clotting
time of the blood for an hour after the ether was first given was
as follows:
9.18--0.5 minute
.19--1 “
.22--1 “
.24--1 “
.26--1 “
.28--1.5 “
.31--1 “
.33--0.5 “
.35--0.5 “
.38--0.5 “
.39--0.5 “
.41--1 “
.43--1 “
.45--0.5 “
.49--0.5 “
.52--0.5 “
.54--0.5 “
.57--1 “
10.00--0.5 “
.02--0.5 “
.06--1 “
.09--0.5 “
.11--0.5 “
.13--1 “
Twenty-four observations made during the hour showed that the
clotting time in this enraged animal averaged three-fourths of a
minute and was never longer than a minute and a half. The clots were
invariably a solid jelly. The persistence of the rapid clotting
for so long a period after anesthesia was started may have been in
part due to continued, rather light, etherization, for Elliott[115]
found that etherization itself could reduce the adrenin content of
the adrenal glands.
The shortened clotting did not always persist so long as in the
foregoing instance. The brief period of faster clotting illustrated
in the following case was typical of many:
Nov. 18.--A cat that had been in stock for some time was placed
on the holder at 2.13, and was at once enraged. Two minutes later
etherization was started. The hairs on the tail were erect. The
clotting was as follows:
2.25--1 minute.
.27--0.5 “
.28--2 “
.31--4.5 “
.37--3.5 “
.47--4.5 “
It seems probable that in this case just as in some of the cases
in which the splanchnic nerves were stimulated (see p. 166), the
adrenals had been well-nigh exhausted because of the cat’s being
caged near dogs, and that the emotional flare-up practically
discharged the glands, for repeated attempts later to reproduce
the initial rapid clotting by stimulation of the splanchnic nerves
were without result.
Evidence presented in previous chapters makes wholly probable the
correctness of the inference that the faster coagulation which
follows emotional excitement is due to adrenal discharge from
splanchnic stimulation. In this relation the effect of severance of
the splanchnics on emotional acceleration of the clotting process
is of interest. The following cases are illustrative:
Oct. 29.--A cat was left on the holder for ten minutes while the
femoral artery was uncovered under local anesthesia. The blood
removed was clotted in a half-minute. The animal was much excited.
It was now quickly etherized and the brain pithed forward from the
neck. The tests resulted as follows:
10.51--1 minute.
.53--0.5 “
.55--0.5 “
.57--0.5 “
11.07 Cut left splanchnic.
.12 “ right splanchnic.
.21--3.5 minutes.
.26--3.5 “
The original record of this case is given in Fig. 34.
[Illustration: Figure 34.--About two-thirds original size. Record
of rapid clotting (less than a half-minute) after emotional
excitement. At 11:07 the left, at 11:12 the right splanchnic
nerves were cut; the clotting then required 3:5 minutes. The marks
below the time record indicate the moments when the samples were
drawn.]
Nov. 5.--A cat was etherized at 2.35. At 2.39 artificial respiration
by tracheal cannula was begun, the air passing through an ether
bottle. The clotting occurred thus:
2.53--1.5 minutes
.57--1.5 “
3.05--1.5 “
.15--1.5 “
.25 Both splanchnics cut and tied in thorax.
.35--4.5 minutes
.55--4.5 “
Nov. 7.--A cat was etherized at 1.55 under excitement and with tail
hairs erect. At 2.13 the animal was showing reflexes. The figures
show the course of the experiment:
2.15--1.5 minutes
.21--1 “
.26--1 “
.31--1 “
.36--1 “
.41--1 “
.46--2 “
.51--2 “
3.06--2 “
.11--2.5 “
.26 Cut left splanchnic in thorax.
.35 Cut right splanchnic in thorax.
.40--5 minutes
.45--5 “
.51--5.5 “
In this instance the subsequent stimulation of the splanchnic nerves
resulted again in faster clotting--a reduction from 5.5 minutes to
3.5 minutes (see experiment Nov. 7, p. 164). The results from this
experiment are expressed graphically in Fig. 35.
[Illustration: Figure 35.--Rapid clotting after emotional
excitement, with slowing of the process when the splanchnic nerves
were cut in the thorax (the left at 3:26, the right at 3:35).]
The data presented in this chapter show that such stimulation
as in the unanesthetized animal would cause pain, and also such
emotions as fear and rage, are capable of greatly shortening the
coagulation time of blood. These results are quite in harmony with
the evidence previously offered that injected adrenin and secretion
from the adrenal glands induced by splanchnic stimulation hasten
clotting, for painful stimulation and emotional excitement also
evoke activity of the adrenals. Here, then, is another fundamental
change in the body, a change tending to the conservation of its
most important fluid, wrought through the adrenal glands in times
of great perturbation. This bodily change and the others which
occur under the same circumstances are next to be examined with
reference to their significance.
REFERENCES
[Footnote 109: Cannon and Mendenhall: American Journal of Physiology,
1914, xxxiv, p. 251.]
[Footnote 110: Macleod: Diabetes: its Pathological Physiology,
London, 1913, pp. 68-72.]
[Footnote 111: Gautrelet and Thomas: Comptes Rendus, Société de
Biologie, 1909, lxvii, p. 233.]
[Footnote 112: Bang: Der Blutzucker, Wiesbaden, 1913, p. 87.]
[Footnote 113: Elliott: Journal of Physiology, 1912, xliv, p. 379.]
[Footnote 114: Elliott: _Loc. cit._, pp. 406, 407.]
[Footnote 115: Elliott: _Loc. cit._, p. 388.]
CHAPTER XI
THE UTILITY OF THE BODILY CHANGES IN PAIN AND GREAT EMOTION
We now turn from a consideration of the data secured in our
experiments to an interpretation of the data. One of the most
important lessons of experience is learning to distinguish between
the facts of observation and the inferences drawn from those facts.
The facts may remain unquestioned; the explanation, however, may
be changed by additional facts or through the influence of more
extensive views. Having given this warning, I propose to discuss
the bearings of the results reported in the earlier chapters.
Our inquiry thus far has revealed that the adrenin secreted by the
adrenal glands in times of stress has all the effects in the body
that are produced by injected adrenin. It plays an essential rôle
in calling forth stored carbohydrate from the liver, thus flooding
the blood with sugar; it helps in distributing the blood to the
heart, lungs, central nervous system and limbs, while taking it away
from the inhibited organs of the abdomen; it quickly abolishes the
effects of muscular fatigue; and it renders the blood more rapidly
coagulable. These remarkable facts are, furthermore, associated
with some of the most primitive experiences in the life of higher
organisms, experiences common to all, both man and beast--the
elemental experiences of pain and fear and rage that come suddenly
in critical emergencies. What is the significance of these profound
bodily alterations? What are the _emergency functions_ of secreted
adrenin?
The Reflex Nature of Bodily Responses in Pain and the
Major Emotions, and the Useful Character of Reflexes
The most significant feature of these bodily reactions in pain
and in the presence of emotion-provoking objects is that they are
of the nature of reflexes--they are not willed movements, indeed
they are often distressingly beyond the control of the will. The
pattern of the reaction, in these as in other reflexes, is deeply
inwrought in the workings of the nervous system, and when the
appropriate occasion arises, typical organic responses are evoked
through inherent automatisms.
It has long been recognized that the most characteristic feature
of reflexes is their “purposive” nature, or their utility either
in preserving the welfare of the organism or in safeguarding it
against injury. The reflexes of sucking, swallowing, vomiting and
coughing, for instance, need only to be mentioned to indicate the
variety of ways in which reflexes favor the continuance of existence.
When, therefore, these automatic responses accompanying pain and
fear and rage--the increased discharge of adrenin and sugar--are
under consideration, it is reasonable to inquire first as to their
utility.
Numerous ingenious suggestions have been offered to account for
the more obvious changes accompanying emotional states--as, for
example, the terrifying aspect produced by the bristling of the
hair and the uncovering of the teeth in an access of rage.[116] The
most widely applicable explanation proposed for these spontaneous
reactions is that during the long course of racial experience they
have been developed for quick service in the struggle for existence.
Earlier writers on organic evolution pointed out the anticipatory
character of these responses. According to Spencer,[117] “Fear, when
strong, expresses itself in cries, in efforts to hide or escape, in
palpitations and tremblings; and these are just the manifestations
that would accompany an actual experience of the evil feared. The
destructive passions are shown in a general tension of the muscular
system, in gnashing of the teeth and protrusion of the claws, in
dilated eyes and nostrils, in growls; and these are weaker forms
of the actions that accompany the killing of prey.” McDougall[118]
has developed this idea systematically and has suggested that
an association has become established between peculiar emotions
and peculiar instinctive reactions; thus the emotion of fear is
associated with the instinct for flight, and the emotion of anger or
rage with the instinct for fighting or attack. Crile[119] likewise
in giving recent expression to the same view has emphasized the
importance of adaptation and natural selection, operative through
myriads of years of racial experience, in enabling us to account
for the already channeled responses which we find established in
our nervous organization. And on a principle of “phylogenetic
association” he assumes that fear, born of innumerable injuries in
the course of evolution, has developed into portentous foreshadowing
of possible injury and has become, therefore, capable of arousing
in the body all the offensive and defensive activities that favor
the survival of the organism.
Because the increase of adrenin and the increase of sugar in the
blood, following painful or strong emotional experiences, are reflex
in character, and because reflexes as a rule are useful responses,
we are justified in the assumption that under these circumstances
these reactions are useful. What, then, is their possible value?
In order that these reactions may be useful they must be _prompt_.
Such is the case. Some observations made by one of my students,
Mr. H. Osgood, show that the latent period of adrenal secretion,
when the splanchnic nerve is stimulated below the diaphragm, is not
longer than 16 seconds; and Macleod[120] states that within a few
minutes after splanchnic stimulation the sugar in the blood rises
between 10 and 30 per cent. The two secretions are, therefore,
almost instantly ready for service.
Conceivably the two secretions might act in conjunction, or each
might have its own function alone. Thus adrenin might serve in
coöperation with nervous excitement to produce increase of blood
sugar, or it might have that function and other functions quite
apart from that. Before these possibilities are considered, however,
the value of the increased blood sugar itself will be discussed.
The Utility of the Increased Blood Sugar as a
Source of Muscular Energy
When we were working on emotional glycosuria a clue to the
significance of the increase of sugar in the blood was found in
McDougall’s suggestion of a relation between “flight instinct”
and “fear emotion,” and “pugnacity instinct” and “anger emotion.”
And the point was made that, since the fear emotion and the anger
emotion are, in wild life, likely to be followed by activities
(running or fighting) which require contraction of great muscular
masses in supreme and prolonged struggle, a mobilization of sugar
in the blood might be of signal service to the laboring muscles.
Pain--and fighting is almost certain to involve pain--would, if
possible, call forth even greater muscular effort. “In the agony
of pain almost every muscle of the body is brought into strong
action,” Darwin[121] wrote, for “great pain urges all animals, and
has urged them during endless generations, to make the most violent
and diversified efforts to escape from the cause of suffering.”[*]
*[Footnote: It is recognized that both pain and the major
emotions may have at times depressive rather than stimulating
effects. For example, Martin and Lacey have shown (American
Journal of Physiology, 1914, xxxiii, p. 212) that such stimuli
as would induce pain may cause a fall of blood pressure, and
they suggest that the rise of blood pressure commonly reported
at times of painful experience is due to the psychic disturbance
that is simultaneously aroused. Conceivably there is a relation
between recognizing the possibility of escape (with the psychic
consequences of that possibility) and the degree of stimulating
effect. Thus pains originating from the interior of the body,
or from injuries sure to be made more painful by action, would
not likely lead to action. On the other hand, the whip and spur
illustrate the well-known excitant effect of painful stimuli.
Similarly in the case of the strong emotions, the effect may be
paralyzing until there is a _definite deed to perform_. Thus
terror may be the most depressing of all emotions, but, as Darwin
pointed out (_Loc. cit._, p. 81), “a man or animal driven through
terror to desperation is endowed with wonderful strength, and is
notoriously dangerous in the highest degree.”]
That muscular work is performed by energy supplied in carbonaceous
material is shown by the great increase of carbon-dioxide output
in severe muscular work, which may exceed twenty times the output
during rest. Furthermore, the storage of glycogen in muscle, and
the disappearance of this glycogen deposit from excised muscle
stimulated to activity,[122] or its reduction after excessive
contractions produced by strychnine,[123] and the lessened ability
of muscles to work if their glycogen store has been reduced,[124]
and the simple chemical relation between sugar and the lactic acid
which appears when muscles are repeatedly made to contract, are all
indications that carbohydrate (sugar and glycogen) is the elective
source of energy for contraction. This conclusion is supported in
recent careful studies by Benedict and Cathcart,[125] who have
shown that a small but distinct increase in the ratio between the
carbon-dioxide breathed out and the oxygen breathed in during a
given period (the respiratory quotient) occurs during muscular
work, and that a decrease in the quotient follows, thus pointing
to a larger proportion of carbohydrate burned during muscular work
than before or after--i. e., a call on the carbohydrate deposits
of the body.
Whether circulating sugar can be immediately utilized by active
muscles has been a subject of dispute. The claim of Chauveau and
Kaufmann[126] that a muscle uses about three and a half times as
much blood sugar when active as when resting, although supported
by Quinquaud,[127] and by Morat and Dufourt,[128] has been denied
by Pavy,[129] who failed to find any difference between the sugar
content of arterial and venous blood when the muscle was contracting;
and also by Magnus-Levy,[130] who has estimated that the amount of
change in sugar content of the blood passing through a muscle must
be so slight as to be within the limits of the error of analysis.
On the other hand, when blood or Ringer’s solution is repeatedly
perfused through contracting heart muscle, the evidence is clear
that the contained sugar may more or less completely disappear.
Thus Locke and Rosenheim[131] found that from 5 to 10 centigrams of
dextrose disappeared from Ringer’s solution repeatedly circulated
through the rabbit heart for eight or nine hours. And recently
Patterson and Starling[132] have shown that if blood is perfused
repeatedly through a heart-lung preparation for three or four
hours, and the heart is continually stimulated by adrenin added
to the blood, the sugar in the blood wholly vanishes; or if the
supply of sugar is maintained, the consumption may rise as high
as 8 milligrams per gram of heart muscle per hour--about four
times the usual consumption. When an animal is eviscerated it may
be regarded as a preparation in which the muscles are perfused
with their proper blood, pumped by the heart and oxygenated by the
lungs. Under these circumstances, the percentage of sugar in the
blood steadily falls,[133] because the utilization by the tissues
is not compensated for by further supply from the liver. Thus,
although there may be doubt that analyses of sugar in the blood
flowing into and out from an active muscle during a brief period
can be accurate enough to prove a clear difference, the evidence
from the experiments above cited shows that when the supply of sugar
is limited it disappears to a greater or less degree when passed
repeatedly through muscular organs.
The argument may be advanced, of course, that the sugar which thus
disappears is not directly utilized, but must first be changed to
glycogen. There is little basis for this assumption. There is, on
the other hand, considerable evidence that increasing the blood
sugar does, in fact, directly increase muscular efficiency. Thus
Locke[134] proved that if oxygenated salt solution is perfused
through the isolated rabbit heart, the beats begin to weaken after
one or two hours; but if now 0.1 per cent dextrose is added to the
perfusing liquid, the beats at once become markedly stronger and
may continue with very slow lessening of strength as long as seven
hours. And Schumberg[135] noted that when he performed a large amount
of general bodily work (thus using up blood sugar) and then tested
flexion of the middle finger in an ergograph, the ability of the
muscle was greater if he drank a sugar solution than if he drank
an equally sweet solution of “dulcin.” He did not know during the
experiment which solution he was drinking. These observations have
been confirmed by Prantner and Stowasser, and by Frentzel.[136] In
experiments on cats, Lee and Harrold[137] found that when sugar is
removed from the animal by means of phlorhizin the _tibialis anticus_
is quickly fatigued; but if, after the phlorhizin treatment, the
animal is given an abundance of sugar and then submitted to the
test, the muscle shows a much larger capacity for work. All this
evidence is, of course, favorable to the view that circulating
sugar may be quickly utilized by contracting muscles.
From the experimental results presented above it is clear that
muscles work preferably by utilizing the energy stored in sugar,
that great muscular labor is capable of considerably reducing the
quantity of stored glycogen and of circulating sugar, and that under
circumstances of a lessened sugar content the increase of blood
sugar considerably augments the ability of muscles to continue
contracting. The conclusion seems justified, therefore, that the
increased blood sugar attendant on the major emotions and pain would
be of direct benefit to the organism in the strenuous muscular
efforts involved in flight or conflict or struggle to be free.
The Utility of Increased Adrenin in the Blood as an
Antidote to the Effects of Fatigue
The function which the discharged adrenin itself might have in
favoring vigorous muscular contraction has already been suggested in
the chapter on the effect of adrenin in restoring the irritability
of fatigued muscle. Some of the earliest evidence proved that
removal of the adrenal glands has a debilitating effect on muscular
power, and that injection of adrenal extract has an invigorating
effect. For these reasons it seemed possible that increased adrenal
secretion, as a reflex result of pain or the major emotions, might
act in itself as a dynamogenic factor in the performance of muscular
work. It was on the basis of that possibility that Nice and I tested
the effect of stimulating the splanchnic nerves (thus causing
adrenal secretion), or injecting adrenin, on the contraction of the
fatigued _tibialis anticus_. We found, as already described, that
when arterial pressure was of normal height, and was prevented from
rising in the legs while the splanchnic was being stimulated, there
was a distinct rise in the height of contraction of the fatigued
muscle. And we drew the inference that adrenin set free in the
blood may operate favorably to the organism by preparing fatigued
muscles for better response to the nervous discharges sent forth
in great excitement.
This inference led to the experiments by Gruber, who examined the
effects of minute amounts of adrenin (0.1 or 0.5 cubic centimeter,
1:100,000), and also of splanchnic stimulation, on the threshold
stimulus of fatigued neuro-muscular and muscular apparatus. Fatigue,
the reader will recall, raises the threshold not uncommonly 100
or 200 per cent, and in some instances as much as 600 per cent.
Rest will restore the normal threshold in periods varying from
fifteen minutes to two hours, according to the length of previous
stimulation. If a small dose of adrenin is given, however, the
normal threshold may be restored in three to five minutes.
From the foregoing evidence the conclusion is warranted that adrenin,
when freely liberated in the blood, not only aids in bringing out
sugar from the liver’s store of glycogen, but also has a remarkable
influence in quickly restoring to fatigued muscles, which have lost
their original irritability, the same readiness for response which
they had when fresh. Thus the adrenin set free in pain and in fear
and rage would put the muscles of the body unqualifiedly at the
disposal of the nervous system; the difficulty which nerve impulses
might have in calling the muscles into full activity would be
practically abolished; and this provision, along with the abundance
of energy-supplying sugar newly flushed into the circulation, would
give to the animal in which these mechanisms are most efficient
the best possible conditions for putting forth supreme muscular
efforts.[*]
*[Footnote: If these results of emotion and pain are not “worked
off” by action, it is conceivable that the excessive adrenin and
sugar in the blood may have pathological effects. (Cf. Cannon:
Journal of the American Medical Association, 1911, lvi, p. 742.)]
The Question Whether Adrenin Normally Secreted Inhibits
the Use of Sugar in the Body
The only evidence opposed to the conclusion which has just been
drawn is that which may be found in results recently reported by
Wilenko. He injected adrenin into urethanized rabbits, usually one
milligram per kilo body weight, and then found that the animals did
not oxidize any part of an intravenous injection of glucose. Rabbits
supplied with glucose in a similar manner, but not given adrenin,
have an increased respiratory quotient. Wilenko[138] concluded,
therefore, that adrenin lessens the capacity of the organism to
burn carbohydrates. In a later paper he reported that adrenin, when
added, with glucose, to physiological salt solution (Locke’s), and
perfused through the isolated rabbit heart, notably increases the
use of sugar by the heart (from 2.2-2.8 to 2.9-4.3 milligrams of
glucose per gram of heart muscle per hour), but that the heart
removed after the animal has received a subcutaneous injection of
adrenin uses much less sugar, only 0.5-1.2 milligrams per gram per
hour. From these results Wilenko[139] concludes that the glycosuria
following injection of adrenin is the result of disturbance of the
use of sugar--an effect which is not direct on the sugar-consuming
organ, but indirect through action on some other organ.
Wilenko’s conclusion fails to account readily for the disappearance
of glycogen from the liver in adrenin glycosuria. Furthermore,
Lusk[140] has recently reported that the subcutaneous administration
of adrenin (one milligram per kilo body weight) to dogs,
simultaneously with 50 grams of glucose by mouth, interferes not at
all with the use of the sugar--the respiratory quotient remains for
several hours at 1.0; i. e., at the figure which glucose alone would
have given. In other words, Lusk’s results with dogs are directly
contradictory to Wilenko’s results with rabbits. Nevertheless,
Wilenko’s conclusion might be quite true for the glycosuria produced
by adrenin alone (which must be excessive), and yet have no bearing
whatever on the glycosuria produced physiologically by splanchnic
stimulation, even though some adrenin is thereby simultaneously
liberated.
The amount of injected adrenin used to produce adrenin glycosuria is
enormous. Osgood has studied in the Harvard Physiological Laboratory
the effects on blood pressure of alternately stimulating the left
splanchnic nerves (with the splanchnic vessels eliminated) and
injecting adrenin, and by this method of comparison[141] has shown
that the amount secreted after five seconds of stimulation varies
between 0.0015 and 0.007 milligram. If 0.005 milligram is taken as
a rather high average figure, and doubled (for two glands), the
amount would be 0.01 milligram. To produce adrenin glycosuria, an
animal weighing two kilos would be injected with two hundred times
this amount. It is granted that more adrenin would be secreted if
the nerves were stimulated longer than five seconds, and that with
injection under the skin or into the abdominal cavity (to produce
glycosuria), the amount of adrenin in the blood at one time would
not be so great as if the injection were into a vein; but even with
these concessions the amount of adrenin in the blood, when it has
been injected to produce glycosuria, is probably very much above
the amount following physiological stimulation of the glands.
Other evidence that the amount of adrenin discharged when the
glands are stimulated is not so great as the amount needed to
produce glycosuria when acting alone is presented in experiments
by Macleod.[142] He found that if the nerve fibres to the liver
were destroyed, stimulation of the splanchnic, which would cause
increased adrenal secretion, did not increase the blood sugar. The
increased blood sugar due to splanchnic stimulation, therefore, is
a nervous effect, dependent, to be sure, on the presence of adrenin
in the blood, but the amount of adrenin present is not in itself
capable of evoking increase.
Furthermore, the increased blood sugar following splanchnic
stimulation may long outlast the stimulation period. The adrenals,
however, as has been demonstrated by Osgood, are soon fatigued, and
fail to respond to repeated stimulation. They seem to be incapable
of prolonged action.
Again, as Macleod[143] has shown, a rise in the sugar content of
the blood can be induced, if the adrenals are intact, merely by
stimulating the nerves going to the liver. The increased blood sugar
of splanchnic origin, therefore, is not due to a disturbance of
the _use_ of sugar in the body, as Wilenko claims for the increase
after adrenin injection, but is a result of a breaking down of the
stored glycogen in the liver and is of nervous origin.
We may conclude, therefore, that since the conditions of Wilenko’s
observations are not comparable with emotional conditions, his
inferences are not pertinent to the present discussion; that when
both adrenin and sugar are increased in the blood as a result of
excitement, the higher percentage of sugar is not due to adrenin
inhibiting the use of sugar by the tissues, and that there is no
evidence at present to show that the brief augmentation of adrenal
discharge, following excitement or splanchnic stimulation, affects
in any deleterious manner the utilization of sugar as a source of
energy. Indeed, the observation of Wilenko and of Patterson and
Starling, above mentioned, that adrenin increases the use of sugar
by the heart, may signify that a _physiological_ discharge of the
adrenals can have a favorable rather than an unfavorable effect on
the employment of sugar by the tissues.
The Vascular Changes Produced by Adrenin
Favorable to Supreme Muscular Exertion
Quite in harmony with the foregoing argument that sugar and adrenin,
which are poured into the blood during emotional excitement, render
the organism more efficient in the physical struggle for existence,
are the vascular changes wrought by increased adrenin, probably in
coöperation with sympathetic innervations. The studies of volume
changes of parts of the body, made by Oliver and Schäfer, have
already been mentioned. Their observations, it will be remembered,
showed that injected adrenin drove the blood from the abdominal
viscera into the organs called upon in emergencies--into the central
nervous system, the lungs, the heart, and the active skeletal
muscles. The absence of effective vasoconstrictor nerves in the
brain and the lungs, and the dilation of vessels in the heart and
skeletal muscles during times of increased activity, make the blood
supply to these parts dependent on the height of general arterial
pressure. In pain and great excitement, as we have already noted,
this pressure is likely to be much elevated, and consequently the
blood flow through the unconstricted or actually dilated vessels
of the body will be all the more abundant.
Adrenin has a well-known stimulating effect on the isolated
heart--causing an increase both in the rate and the amplitude of
cardiac contraction. This effect accords with the general rule that
adrenin simulates the action of sympathetic impulses. It is commonly
stated, however, that if the heart holds its normal relations
in the body, adrenin causes slowing of the beat.[144] This view
is doubtless due to the massive doses that have been employed,
which are quite beyond physiological limits and which induce such
enormous increases of arterial pressure that the natural influence
of adrenin on heart muscle is overcome by mechanical obstacles to
quick contractions and by inhibitory impulses from the central
nervous system. Hoskins and Lovellette have recently shown that when
the precaution is taken to inject adrenin into a vein in a manner
resembling the discharge from the adrenal glands, not only is there
increased blood pressure, but generally, also, an acceleration of
the pulse.[145] At the same time, therefore, that a greater amount
of work, from increased arterial pressure, is demanded of the
heart, blood is delivered to the heart in greater abundance, and
the muscle is excited to more rapid and vigorous pulsations. The
augmentation of the heart beat is thus coördinate with the other
adaptive functions of the adrenal glands in great emergencies.
The Changes in Respiratory Function Also
Favorable to Great Effort
The urgent need in struggle or flight is a generous supply of
oxygen to oxidize the metabolites of muscular contraction, and a
quick riddance of the resultant carbon-dioxide from the body. The
moment vigorous exercise is begun the breathing at once changes
so as to bring about a more thorough ventilation of the lungs.
And one of the most characteristic reactions of animals in pain
and emotional excitement is deep and rapid respiration. Again the
reflex response is precisely what would be most serviceable to the
organism in the strenuous efforts of fighting or escape that might
accompany or follow distress or fear or rage. It is known that by
such forced respirations the carbon-dioxide content of the blood
can be so much reduced that the need for any breathing whatever
may be deferred for as much as a minute or even longer.[146] And
Douglas and Haldane[147] have found that moderately forced breathing
for three minutes previous to severe muscular exertion results in
greatly diminishing the subsequent respiratory distress, as well as
lessening the amount of air breathed and the amount of carbon-dioxide
given off. Furthermore, the heart beats less rapidly after the
performance and returns more quickly from its increased rate to
normal. The forced respirations in deeply emotional experiences
can be interpreted, therefore, as an anticipatory reduction of
the carbon-dioxide in the blood, a preparation for the augmented
discharge of carbon-dioxide into the blood as soon as great muscular
exertion begins.[*]
*[Footnote: The excessive production of heat in muscular work
gives rise to sweating. The evaporation of sweat helps to keep the
body temperature from rising unduly from the heat of exertion.
Again in strong emotion and in pain the “cold sweat” that appears
on the skin may be regarded as a reaction anticipatory of the
strenuous muscular movements that are likely to ensue.]
As the air moves to and fro in the lungs with each respiration, it
must pass through the fine divisions of the air tubes or bronchioles.
The bronchioles are provided with smooth muscle, which, in all
probability, like smooth muscle elsewhere in the body, is normally
held in a state of tonic contraction. When this tonic contraction
is much increased, as in asthma, breathing becomes difficult, and
even with the body at rest unusual effort is then required to
maintain the minimal necessary ventilation of the lungs. During
strenuous exertion, with each breath the air must rush through the
bronchioles in greatly increased volume and speed. Thus in a well
person “winded” with running, for example, the bronchioles might
become _relatively_ too small for the stream of air, just as they
are too small in a person ill with asthma. And then some extra
energy would have to be expended to force the air back and forth
with sufficient rapidity to satisfy the bodily needs. It is probable
that even under the most favorable conditions, the labored breathing
in hard exercise involves to some degree the work of accelerating
the tidal flow of the respiratory gases. This extra labor would
obviously be reduced, if the tonic contraction of the ring-muscles
in the wall of the bronchioles was reduced, so that the tubules were
enlarged. It has been shown by a number of investigators, who have
used various methods, that adrenin injected into the blood stream has
as one of its precise actions the dilating of the bronchioles.[148]
The adrenin discharged in emotional excitement goes to the lungs
before entering into relation with any other organ except the
right heart chamber; it may, therefore, have as its first effect
the relaxation of the smooth muscles of the lungs. This would be
another very direct means of rendering the organism more efficient
when fierce struggle calls for a bounteous supply of fresh air and
a speedy discharge of the carbonaceous waste.
Effects Produced in Asphyxia Similar to Those Produced
in Pain and Excitement
All the bodily responses occurring in pain and emotional excitement
have thus far been considered as _anticipatory_ of the instinctive
acts which naturally follow. And as we have seen, these responses can
reasonably be interpreted as preparatory to the great exertions which
may be demanded of the organism. This interpretation of the facts
is supported by the discovery that a mechanism exists whereby the
changes initiated in an anticipatory manner by emotional excitement
are continued or perhaps augmented by the exertion itself.
Great exertion, such as might attend flight or conflict, would
result in an excessive production of carbon-dioxide. Then, although
respiratory and circulatory changes of emotional origin may have
prepared the body for struggle, the emotional provisions for keeping
the working parts at a high level of efficiency may not continue to
operate, or they may not be adequate. If there is painful gasping
for breath in the course of prolonged and vigorous exertion, or
for a considerable period after the work has ceased, a condition
of partial asphyxia has evidently been induced. This condition, as
everyone knows, is distinctly unfavorable to further effort. But
the asphyxia itself may act as a stimulus.[149]
In our examination of the influence of various conditions on the
secretion of the adrenal glands, Hoskins and I[150] tested the
effects of asphyxia. By use of the intestinal segment as an indicator
we compared the action of blood, taken as nearly simultaneously
as possible from the vena cava above the adrenal vessels and from
the femoral vein before asphyxia, with blood taken from the same
sources after asphyxia had been produced. The femoral venous blood
after passing the capillaries of the leg thus acted as a standard
for the same blood after receiving the contribution of the adrenal
veins. Asphyxia was caused by covering the tracheal cannula until
respiration became labored and slow, but capable of recovery when
air was admitted. It may be regarded, therefore, as not extreme.
The results of the degree of asphyxia above described are shown
by graphic record in Fig. 36. Blood taken from the vena cava and
from the femoral vein before asphyxia (“normal”) failed to cause
inhibition of the contractions. Blood taken from the femoral vein
after asphyxia produced almost the same effect as blood from the same
vein before; asphyxia, therefore, had wrought no change demonstrable
in the general venous flow. Blood taken from the vena cava after
asphyxia had, on the contrary, an effect markedly unlike blood
from the same region before (compare the record after 1 and after
7, Fig. 36)--it caused the typical inhibition which indicates the
presence of adrenal secretion.[*]
[Illustration: Figure 36.-- At 1 normal vena-cava blood applied,
at 2 removed. At 3 normal blood from femoral vein applied, at 4
removed. At 5 blood from femoral vein after asphyxia applied, at
6 removed. At 7 blood from the vena cava after asphyxia applied.
Time, half-minutes.]
*[Footnote: This positive result might suggest that the comparison
of both femoral and vena-cava blood under each condition was
unnecessary, and that a comparison merely of vena-cava blood
before and after asphyxia would be sufficient. Positive results
were indeed thus secured, but they occurred even when the adrenal
glands were carefully removed and extreme asphyxia (i. e.,
stoppage of respiration) was induced. That the blood may contain
in extreme asphyxia a substance or substances capable of causing
inhibition of intestinal contractions was thus demonstrated. In
one instance, after the blood was proved free from adrenin, the
aorta and vena cava were tied close below the diaphragm, and the
carotids were tied about midway in the neck. Extreme asphyxia
was produced (lasting five minutes). Blood now taken from the
heart caused marked inhibition of the beating intestinal segment.
Probably, therefore, the inhibitory action of blood taken from
an animal when _extremely_ asphyxiated cannot be due to adrenin
alone.]
That the positive result obtained in moderate asphyxia is not
attributable to other agencies in the blood than adrenin is indicated
by the failure of asphyxial femoral blood to cause inhibition, while
vena-cava blood, taken almost simultaneously, brought about immediate
relaxation of the muscle. The conclusion was drawn, therefore, that
asphyxia results in increased secretion of the adrenal glands.
This conclusion has been supported by Borberg and Fridericia,[151]
and also by Starkenstein,[152] who found that an increase of
carbon-dioxide in the blood lessens the adrenin in the adrenal
medulla. And recently Czubalski[153] also has inferred, from the
rise of blood pressure in asphyxia when the adrenals are intact and
the absence of the rise if the adrenals are removed, that asphyxia
sets free adrenin in the blood.
Asphyxia, like pain and excitement, not only liberates adrenin, but,
as might be inferred from that fact, also mobilizes sugar.[154]
And, furthermore, Starkenstein[155] has shown that the asphyxia
due to carbon-monoxide poisoning is not accompanied by increased
blood sugar if the adrenal glands have been removed.
In case strong emotions are followed by vigorous exertions,
therefore, asphyxia is likely to result, and this will act in
conjunction with the emotional excitement and pain, or perhaps in
continuation of the influences of these states, to bring forth
still more adrenal discharge and still further output of sugar from
the liver. And these in turn would serve the laboring muscles in
the manner already described. This suggestion is in accord with
Macleod’s[156] that the increased freeing of glycogen from the liver
produced by muscular exercise is possibly associated with increased
carbon-dioxide in the blood. And it also harmonizes with Zuntz’s
statement[157] that the asphyxia of great physical exertion may
call out sugar to such a degree that, in spite of the increased
use of it in the active muscles, glycosuria may ensue.
The evidence previously adduced that adrenin causes relaxation of
the smooth muscle of the bronchioles, taken in conjunction with the
evidence that adrenal secretion is liberated in asphyxia, suggests
that relief from difficult breathing may thus be automatically
provided for in the organism. The well-known phenomenon of “second
wind” is characterized by an almost miraculous refreshment and
renewal of vigor, after an individual has persisted in violent
exertion in spite of being “out of breath.” It seems not improbable
that this phenomenon, for which many explanations have been offered,
is really due to setting in operation the supporting mechanism which,
as we have seen, plays so important a rôle in augmenting bodily
vigor in emotional excitement. The release of sugar and adrenin,
the abundance of blood flow through the muscles--supplying energy
and lessening fatigue--and the relaxation of the bronchiolar walls,
are all occurrences which may reasonably be regarded as resulting
from asphyxia. And when they take place they doubtless do much to
abolish the distress itself by which they were occasioned. According
to this explanation “second wind” would consist in the establishment
of the same group of bodily changes, leading to more efficient
physical struggle, that are observed in pain and excitement.
The Utility of Rapid Coagulation in
Preventing Loss of Blood
The increase of blood sugar, the secretion of adrenin, and the
altered circulation in pain and emotional excitement have been
interpreted in the foregoing discussion as biological adaptations
to conditions in wild life which are likely to involve pain and
emotional excitement, i. e., the necessities of fighting or flight.
The more rapid clotting of blood under these same circumstances may
also be regarded as an adaptive process, useful to the organism.
The importance of conserving the blood, especially in the struggles
of mortal combat, needs no argument. The effect of local injury
in favoring the formation of a clot to seal the opened vessels is
obviously adaptive in protecting the organism against hemorrhage.
The injury that causes opening of blood vessels, however, is, if
extensive, likely also to produce pain. And, as already shown,
conditions producing pain increase adrenal secretion and hasten
coagulation. Thus injury would be made less dangerous as an occasion
for serious hemorrhage by two effects which the injury itself
produces in the body--the local effect on clotting at the region
of injury and the general effect on the speed of clotting wrought
by reflex secretion of adrenin.
According to the argument here presented the strong emotions, as
fear and anger, are rightly interpreted as the concomitants of
bodily changes which may be of utmost service in subsequent action.
These bodily changes are so much like those which occur in pain
and fierce struggle that, as early writers on evolution suggested,
the emotions may be considered as foreshadowing the suffering and
intensity of actual strife. On this general basis, therefore, the
bodily alterations attending violent emotional states would, as
organic preparations for fighting and possible injury, naturally
involve the effects which pain itself would produce. And increased
blood sugar, increased adrenin, an adapted circulation and rapid
clotting would all be favorable to the preservation of the organism
that could best produce them.
REFERENCES
[Footnote 116: See Darwin: Expression of Emotions in Man and Animals,
New York, 1905, pp. 101, 117.]
[Footnote 117: Spencer: Principles of Psychology, London, 1855.]
[Footnote 118: McDougall: Introduction to Social Psychology, London,
1908, pp. 49, 59.]
[Footnote 119: Crile: Boston Medical and Surgical Journal, 1910,
clxiii, p. 893.]
[Footnote 120: Macleod: Diabetes, etc., p. 80.]
[Footnote 121: Darwin: _Loc. cit._, p. 72.]
[Footnote 122: Nasse: Archiv für die gesammte Physiologie, 1869,
ii, p. 106; 1877, xiv, p. 483.]
[Footnote 123: Frentzel: Archiv für die gesammte Physiologie, 1894,
lvi, p. 280.]
[Footnote 124: Zuntz: Oppenheimer’s Handbuch der Biochemie, Jena,
1911, iv (first half), p. 841.]
[Footnote 125: Benedict and Cathcart: Muscular Work, a Metabolic
Study, Washington, 1913, pp. 85-87.]
[Footnote 126: Chauveau and Kaufmann: Comptes Rendus, Académie des
Sciences, 1886, ciii, p. 1062.]
[Footnote 127: Comptes Rendus, Société de Biologie, 1886, xxxviii,
p. 410.]
[Footnote 128: Morat and Dufourt: Archives de Physiologie, 1892,
xxiv, p. 327.]
[Footnote 129: Pavy: The Physiology of the Carbohydrates, London,
1894, p. 166.]
[Footnote 130: Magnus-Levy: v. Noorden’s Handbuch der Pathologie
des Stoffwechsels, 1906, i, p. 385.]
[Footnote 131: Locke and Rosenheim: Journal of Physiology, 1907,
xxxvi, p. 211.]
[Footnote 132: Patterson and Starling: Journal of Physiology, 1913,
xlvii, p. 143.]
[Footnote 133: See Macleod and Pearce: American Journal of
Physiology, 1913, xxxii, p. 192. Pavy and Siau: Journal of
Physiology, 1903, xxix, p. 375. Macleod: American Journal of
Physiology, 1909, xxiii, p. 278.]
[Footnote 134: Locke: Centralblatt für Physiologie, 1900, xiv, p.
671.]
[Footnote 135: Schumberg: Archiv für Physiologie, 1896, p. 537.]
[Footnote 136: Frentzel: Archiv für Physiologie, 1899, Supplement
Band, p. 145.]
[Footnote 137: Lee and Harrold: American Journal of Physiology,
1900, iv, p. ix.]
[Footnote 138: Wilenko: Biochemische Zeitschrift, 1912, xlii, p.
58.]
[Footnote 139: Wilenko: Archiv für experimentelle Pathologie und
Pharmakologie, 1913, lxxi, p. 266.]
[Footnote 140: Lusk: Proceedings of the Society for Experimental
Biology and Medicine, 1914, xi, p. 49. Also Lusk and Riche: Archives
of Internal Medicine, 1914, xiii, p. 68.]
[Footnote 141: See Elliott: Journal of Physiology, 1912, xliv, p.
376.]
[Footnote 142: Macleod: Diabetes, etc., pp. 64-73.]
[Footnote 143: Macleod: Diabetes, etc., pp. 68-72.]
[Footnote 144: See Biedl: Die Innere Sekretion, 1913, i, p. 464.]
[Footnote 145: Hoskins and Lovellette: Journal of the American
Medical Association, 1914, lxiii, p. 317.]
[Footnote 146: See Haldane and Priestley: Journal of Physiology,
1905, xxxii, p. 255.]
[Footnote 147: Douglas and Haldane: Journal of Physiology, 1909,
xxxix, p. 1.]
[Footnote 148: See Januschke and Pollak: Archiv für experimentelle
Pathologie und Pharmakologie, 1911, lxvi, p. 205. Trendelenburg:
Zentralblatt für Physiologie, 1912, xxvi, p. 1. Jackson: Journal
of Pharmacology and Experimental Therapeutics, 1912, iv, p. 59.]
[Footnote 149: Cf. Hoskins and McClure: Archives of Internal
Medicine, 1912, x, p. 355.]
[Footnote 150: Cannon and Hoskins: American Journal of Physiology,
1911, xxix, p. 275.]
[Footnote 151: Borberg: Skandinavisches Archiv für Physiologie,
1913, xxviii, p. 125.]
[Footnote 152: Starkenstein: Zeitschrift für experimentelle
Pathologie und Therapie, 1911, x, p. 95.]
[Footnote 153: Czubalski: Zentralblatt für Physiologie, 1913, xxvii,
p. 580.]
[Footnote 154: For evidence and for references to this literature,
see Bang: Der Blutzucker, Wiesbaden, 1913, pp. 104-108.]
[Footnote 155: Starkenstein: _Loc. cit._, p. 94.]
[Footnote 156: Macleod: Diabetes, etc., p. 184.]
[Footnote 157: Zuntz: _Loc. cit._, p. 854.]
CHAPTER XII
THE ENERGIZING INFLUENCE OF EMOTIONAL EXCITEMENT
The close relation between emotion and muscular action has long been
perceived. As Sherrington[158] has pointed out, “Emotion ‘moves’ us,
hence the word itself. If developed in intensity, it impels toward
vigorous movement. Every vigorous movement of the body ... involves
also the less noticeable coöperation of the viscera, especially of
the circulatory and respiratory. The extra demand made upon the
muscles that move the frame involves a heightened action of the
nutrient organs which supply to the muscles the material for their
energy.” The researches here reported have revealed a number of
unsuspected ways in which muscular action is made more efficient
because of emotional disturbances of the viscera. Every one of the
visceral changes that have been noted--the cessation of processes
in the alimentary canal (thus freeing the energy supply for other
parts); the shifting of blood from the abdominal organs, whose
activities are deferable, to the organs immediately essential to
muscular exertion (the lungs, the heart, the central nervous system);
the increased vigor of contraction of the heart; the quick abolition
of the effects of muscular fatigue; the mobilizing of energy-giving
sugar in the circulation--every one of these visceral changes is
_directly serviceable in making the organism more effective in the
violent display of energy which fear or rage or pain may involve_.
“Reservoirs of Power”
That the major emotions have an energizing effect has been commonly
recognized.[*] Darwin testified to having heard, “as a proof of
the exciting nature of anger, that a man when excessively jaded
will sometimes invent imaginary offences and put himself into a
passion, unconsciously for the sake of reinvigorating himself;
and,” Darwin[159] continues, “since hearing this remark, I have
occasionally recognized its full truth.” Under the impulse of
fear also, men have been known to achieve extraordinary feats of
running and leaping. McDougall[160] cites the instance of an
athlete who, when pursued as a boy by a savage animal, leaped over
a wall which he could not again “clear” until he attained his full
stature and strength. The very unusual abilities, both physical
and mental, which men have exhibited in times of stress were dealt
with from the psychological point of view by William James[161] in
one of his last essays. He suggested that in every person there
are “reservoirs of power” which are not ordinarily called upon,
but which are nevertheless ready to pour forth streams of energy
if only the occasion presents itself. These figurative expressions
of the psychologist receive definite and concrete exemplification,
so far as the physical exhibitions of power are concerned, in the
highly serviceable bodily changes which have been described in the
foregoing chapters.
*[Footnote: Russell (The Pima Indians, United States Bureau of
Ethnology, 1908, p. 243) relates a tale told by the Indians to
their children, in which an injured coyote was chasing some quails.
“Finally the quails got tired,” according to the story, “but the
coyote did not, for he was angry and did not feel fatigue.”]
It would doubtless be incorrect to attempt to account for all the
increased strength and tireless endurance, which may be experienced
in periods of great excitement, on the basis of abundant supplies
provided then for muscular contraction, and a special secretion for
avoiding or abolishing the depressive influences of fatigue. Tremors,
muscular twitchings, the assumption of characteristic attitudes,
all indicate that there is an immensely augmented activity of the
nervous system--an activity that discharges powerfully even into
parts not directly concerned in struggle, as, for example, into
the muscles of voice, causing peculiar cries or warning notes; into
the muscles of the ears, drawing them back or causing them to stand
erect, and into the small muscles about the lips, tightening them
and revealing the teeth. The typical appearances of human beings,
as well as lower animals, when in the grip of such deeply agitating
emotions as fear and rage, are so well recognized as to constitute a
primitive and common means of judging the nature of the experience
through which the organism is passing. This “pattern” response of
the nervous system to an emotion-provoking object or situation is
probably capable of bringing into action a much greater number
of neurones in the central nervous system than are likely to be
concerned in even a supreme act of volition. The nervous impulses
delivered to the muscles, furthermore, operate upon organs well
supplied with energy-yielding material and well fortified by rapidly
circulating blood and by secreted adrenin, against quick loss of
power because of accumulating waste. Under such circumstances of
excitement the performance of extraordinary feats of strength or
endurance is natural enough.[*]
*[Footnote: If individual neurones obey the law of either supreme
action or inaction, the “all-or-none law,” the only means of
securing a graded response is through variation of the _number_ of
neurones engaged in action--the more, the greater the resulting
manifestation of strength.]
In connection with the conception that strong emotion has a
dynamogenic value, it is of interest to note that on occasions
when great demands are likely to be placed on the neuro-muscular
system in the doing of unusual labors, emotional excitement is not
uncommonly an accompaniment. In order to emphasize points in the
argument developed thus far, I propose to cite some examples of the
association of emotional excitement with remarkable exhibitions of
power or resistance to fatigue.
The Excitements and Energies of Competitive Sports
Already in an earlier account (see p. 75) I have mentioned finding
sugar in the urine in approximately fifty per cent of a group of
college football players after the most exacting game of the season’s
play. As is well understood, such games are heralded far and wide,
loyal supporters of each college may travel hundreds of miles to
attend the contest, enthusiastic meetings of undergraduate students
are held in each college to demonstrate their devotion to the team
and their confidence in its prowess--indeed, the arguments for
victory, the songs, the cheering, are likely to be so disturbing
to the players, that before an important contest they are not
infrequently removed from college surroundings in order to avoid
being overwrought when the contest comes.
On the day of the contest the excitement is multiplied manyfold.
There is practically a holiday in college and to a large extent
in the city as well. The streets are filled with eager supporters
of each team as the hosts begin to gather at the field. As many
as 70,000 spectators may be present, each one tense and strongly
partisan. The student bands lead the singing, by thousands of
voices, of songs which urge to the utmost effort for the college;
and, in anticipation, these songs also celebrate the victory.
Into the midst of that huge, cheering, yelling, singing, flag-waving
crowd, the players are welcomed in a special outburst of these same
demonstrations of enthusiasm. Soon the game begins. The position
of every player is known, if not because of previous acquaintance
and recognition, because card-diagrams give the information. Every
important play is seen by the assembled thousands, and the player who
makes it is at once announced to all, and is likely to be honored
by his multitudinous college mates in a special cheer, ending in
his name. Any player who, by infraction of the rules or failure to
do his part, loses ground gained by his team is also known. The man
who is “played out” in efforts to win for his team and college,
and consequently has to leave the field, is welcomed to the side
lines by acclamations suited for a great hero. In short, every
effort is made, through the powerful incentives of censure and
a flaunting recognition, to make each member of the team realize
vividly his responsibility, both personal and as one of a group,
for the supreme, all-important result--victory for his college.
This responsibility works tremendously on the emotions of the
players. In the dressing room before a critical contest I have seen a
“gridiron warrior,” ready in canvas suit, cleated shoes, and leather
helmet, sitting grimly on a bench, his fists clenched, his jaws
tight, and his face the color of clay. He performed wonderfully when
the game began, and after it was over there was a large percentage
of sugar in his urine! Probably no sport requires a more sustained
and extreme display of neuro-muscular effort than American football.
And from the foregoing description of the conditions that surround
the contests it is easy to realize that they conspire to arouse in
the players excitements which would bring forth very efficiently
the bodily reserves for use in the fierce struggle which the game
requires.
What is true of football is true, though perhaps to a less degree,
of the racing sports, as running and rowing. Again great multitudes
attend the events, the contests are followed closely from beginning
to end, and as the goal is approached the cheering and cries for
victory gather in volume and intensity as if arranged for a thrilling
climax. The whole setting is most highly favorable to the dramatic
development of an acme of excitement as the moment for the last
desperate effort to win is put forth.
Frenzy and Endurance in Ceremonial and Other Dances
Dancing, which formed a significant feature of primitive rituals, has
always been accompanied by exciting conditions, and not unusually
was an exhibition of remarkable endurance. In the transfer of the
Ark to Zion there were processions and sacrifices, and King David
“danced before the Lord with all his might.” Mooney[162] in his
account of dances among the American Indians tells of a young man
who in one of the ceremonials danced three days and nights without
food, drink or sleep. In such a terrible ordeal the favoring
presence of others, who through group action help to stimulate both
the excitement and the activities, must be an important element in
prolonging the efforts of the individual.
In the history of religious manias[163] there are many instances
of large numbers of people becoming frenzied and then showing
extraordinary endurance while dancing. In 1374 a mania broke forth
in Germany, the Netherlands and France, in which the victims claimed
to dance in honor of Saint John. Men and women went about dancing
hand in hand, in pairs, or in a circle, on the streets, in the
churches, at their homes, or wherever they might be, hour after
hour without rest. While dancing they sang, uttered cries, and
saw visions. Whole companies of these crazy fanatics went dancing
along the public roads and into the cities, until they had to be
interfered with.
In 1740 an extraordinary sect, known as the “Jumpers,” arose in
Wales. According to the description given by Wesley, their exercises
were not unlike those of certain frenzied states among the Indians.
“After the preaching was over,” Wesley[164] wrote, “anyone who
pleased gave out a verse of a hymn; and this they sung over and
over again, with all their might and main, thirty or forty times,
till some of them worked themselves into a sort of drunkenness
or madness; they were then violently agitated, and leaped up and
down in all manner of postures, frequently for hours together.”
There were sometimes thousands at a single meeting of the Jumpers,
shouting out their excitement and ready to leap for joy.[165] Wesley
has also described instances of tremendous emotional outburst at
Methodist meetings which he addressed. “Some were torn with a kind
of convulsive motion in every part of their bodies, and that so
violently that often four or five persons could not hold one of
them. I have seen many hysterical or epileptic fits,” he wrote,
“but none of them were like these in many respects.”
Among the dervishes[166] likewise the dance is accompanied by
intense excitement and apparently tireless movements. “The cries
of ‘Yâ Allah!’ are increased doubly, as also those of ‘Yâ Hoo!’
with frightful howlings shrieked by the dervishes together in the
dance.”... “There was no regularity in their dancing, but each seemed
to be performing the antics of a madman; now moving his body up and
down; the next moment turning round, then using odd gesticulations
with his arms, next jumping, and sometimes screaming.”... “At the
moment when they would seem to stop from sheer exhaustion the sheikh
makes a point of exciting them to new efforts by walking through
their midst, making also himself most violent movements. He is next
replaced by two elders, who double the quickness of the step and
the agitation of the body; they even straighten themselves up from
time to time, and excite the envy or emulation of others in their
astonishing efforts to continue the dance until their strength is
entirely exhausted.” Such is the frenzy thus developed that the
performers may be subjected to severe pain, yet only show signs of
elation.
In all these dances the two most marked features are the intense
excitement of those who engage in them and the very remarkable
physical endurance which they manifest. Although there is no direct
evidence, such as was obtained in examining the football players,
that bodily changes favorable to great neuro-muscular exertion are
developed in these furies of fanaticism, it is highly probable that
they are so developed, and that the feats of fortitude which are
performed are to a large extent explicable on the basis of a “tapping
of the reservoirs of power” through the emotional excitement.
The Fierce Emotions and Struggles of Battle
Throughout the discussion of the probable significance of the bodily
changes in pain and great emotion, the value of these changes in the
struggles of conflict or escape was emphasized. In human beings as
well as in lower animals the wildest passions are aroused when the
necessities of combat become urgent. One needs only to glance at
the history of warfare to observe that when the primitive emotions
of anger and hatred are permitted full sway, men who have been
considerate and thoughtful of their fellows and their fellows’ rights
suddenly may turn into infuriated savages, slaughtering innocent
women and children, mutilating the wounded, burning, ravaging, and
looting, with all the wild fervor of demons. It is in such excesses
of emotional turbulence that the most astonishing instances of
prolonged exertion and incredible endurance are to be found.
Probably the fiercest struggles between men that are recorded are
those which occurred when the wager of battle was a means of
determining innocence or guilt. In the corners of the plot selected
for the combat a bier was prepared for each participant, as a symbol
that the struggle was for life or death. Each was attended by his
relatives and followers, and by his father confessor.[167] After
each had prayed to God for help in the coming combat, the weapons
were selected, the sacrament was administered, and the battle was
begun. The principals fought to the end with continuous and brutal
ferocity, resembling the desperate encounters of wild beasts. A
fairly illustrative example is furnished in an incident which
followed the assassination of Charles the Good of Flanders in 1127.
One of the accomplices, a knight named Guy, was challenged for
complicity by another named Herman. Both were renowned warriors.
Herman was speedily unhorsed by Guy, who with his lance frustrated
all Herman’s attempts to remount. Then Herman disabled Guy’s horse,
and the combat was renewed on foot with swords. Equally skilful in
fence, they continued the struggle till fatigue compelled them to
drop sword and shield, whereupon they wrestled for the mastery. Guy
threw his antagonist, fell on him, and beat him in the face with his
gauntlets till he seemed to be motionless; but Herman had quietly
slipped his hand below the other’s coat of mail and, grasping the
testicles, with a mighty effort wrenched them away. Immediately
Guy fell over and expired.[168] In such terrific fights as these,
conducted in the extremes of rage and hate, the mechanisms for
reënforcing the parts of the body which are of primary importance
in the struggle are brought fully into action and are of utmost
value in securing victory.
The Stimulating Influence of Witnesses and of Music
It is noteworthy that in all the instances thus far cited--in the
great games, in dancing, and in fighting--two factors are present
that are well known to have an augmenting effect both in the full
development of emotions and in the performance of unusual muscular
labors. One of these is the crowd of witnesses or participants, who
contribute the “mob spirit” that tends to carry the actions of the
individual far beyond the limits set by any personal considerations
or prudencies. The other is the influence of music. As Darwin long
ago indicated, music has a wonderful power of recalling in a vague
and indefinite manner strong emotions which have been felt by our
ancestors in long-past ages. Especially is this true of martial
music. For the grim purposes of war the reed and the lute are
grotesquely ill-suited; to rouse men to action strident brass and
the jarring instruments of percussion are used in full force. The
influence of martial music on some persons is so profound as to
cause the muscles to tremble and tears to come to the eyes--both
indications of the deep stirring of emotional responses in the body.
And when deeds of fortitude and fierce exertion are to be performed
the effectiveness of such music in rousing the aggressive emotions
has long been recognized. The Romans charged their foes amid the
blasts of trumpets and horns. The ancient Germans rushed to battle,
their forces spurred by the sounds of drums, flutes, cymbals and
clarions. There is a tradition that the Hungarian troops are the
worst in Europe, until their bands begin to play--then they are the
best! The late General Linevitch is quoted as saying: “Music is one
of the most vital ammunitions of the Russian army. Without music a
Russian soldier would be dull, cowardly, brutal and inefficient.
From music he absorbs a magic power of endurance, and forgets the
sufferings and mortality. It is a divine dynamite.” And Napoleon
is said to have testified that the weird and barbaric tunes of the
Cossack regiments infuriated them to such rage that they wiped out
the cream of his army.[169] A careful consideration of the use of
martial music in warfare would perhaps bring further interesting
evidence that its function is to reënforce the bodily changes that
attend the belligerent emotions.
Only a few instances of the combination of extreme pain, rage, terror
or excitement, and tremendous muscular power have been given in the
preceding pages. Doubtless in numerous other conditions these two
groups of phenomena occur together. In the lives of firemen and the
police, in the experiences of escaping prisoners, of shipwrecked
sailors, in the struggles between pioneers and their savage enemies,
in accounts of forced marches or retreats, search would reveal
many examples of such bodily disturbances as have been described
in earlier chapters as augmenting the effectiveness of muscular
efforts, and such exhibitions of power or endurance as are evidently
far beyond the ordinary. There is every reason for believing that,
were the conditions favorable to experimental testing, it would
be possible to demonstrate and perhaps to measure the addition to
the dynamics of bodily action that appears as the accompaniment of
violent emotional disturbance.
The Feeling of Power
In this connection it is highly significant that in times of
strong excitement there is not infrequent testimony to a sense of
overwhelming power that sweeps in like a sudden tide and lifts the
person to a new high level of ability. A friend of mine, whose
nature is somewhat choleric, has told me that when he is seized
with anger, he is also possessed by an intense conviction that he
could crush and utterly destroy the object of his hostility. And
I have heard a football player confess that just before the final
game such an access of strength seemed to come to him that he felt
able, on the signal, to crouch and with a jump go crashing through
any ordinary door. There is intense satisfaction in these moments
of supreme elation, when the body is at its acme of accomplishment.
And it is altogether probable that the critical dangers of adventure
have a fascination because fear is thrilling, and extrication from a
predicament, by calling forth all the bodily resources and setting
them to meet the challenge of the difficulty, yields many of the
joys of conquest. For these reasons vigorous men go forth to seek
dangers and to run large chances of serious injury. “Danger makes
us more alive. We so love to strive that we come to love the fear
that gives us strength for conflict. Fear is not only something
to be escaped from to a place or state of safety, but welcomed as
an arsenal of augmented strength.”[170] And thus in the hazardous
sports, in mountain climbing, in the hunting of big game, and in
the tremendous adventure of war, risks and excitement and the sense
of power surge up together, setting free unsuspected energies, and
bringing vividly to consciousness memorable fresh revelations of
the possibilities of achievement.
REFERENCES
[Footnote 158: Sherrington: The Integrative Action of the Nervous
System, New York, 1906, p. 265.]
[Footnote 159: Darwin: The Expression of Emotions in Man and Animals,
New York, 1905, p. 79.]
[Footnote 160: McDougall: Introduction to Social Psychology, London,
1908, p. 50.]
[Footnote 161: James: The Energies of Men, p. 227, in Memories and
Studies, New York, 1911.]
[Footnote 162: Mooney: The Ghost-Dance Religion, United States
Bureau of Ethnology, 1892-3, p. 924.]
[Footnote 163: Schaff: Religious Encyclopedia, New York, 1908, iii,
p. 346.]
[Footnote 164: Southey: Life of Charles Wesley, New York, 1820,
ii, p. 164.]
[Footnote 165: Southey: _Loc. cit._, i, p. 240.]
[Footnote 166: Brown: The Dervishes, London, 1868, pp. 218-222,
260.]
[Footnote 167: Majer: Geschichte der Ordalien, Jena, 1796, pp.
258-261.]
[Footnote 168: Lea: Superstition and Force, Philadelphia, 1892, p.
178.]
[Footnote 169: Narodny: Musical America, 1914, xx, No. 14.]
[Footnote 170: Hall: American Journal of Psychology, 1914, xxv, p.
154.]
CHAPTER XIII
THE NATURE OF HUNGER
On the same plane with pain and the dominant emotions of fear
and anger, as agencies which determine the action of organisms,
is the sensation of hunger. It is a sensation so peremptory, so
disagreeable, so tormenting, that men have committed crimes in order
to assuage it. It has led to cannibalism, even among the civilized.
It has resulted in suicide. And it has defeated armies--for the
aggressive spirit becomes detached from larger loyalties and turns
personal and selfish as hunger pangs increase in vigor and insistence.
In 1905, while observing in myself the rhythmic sounds produced by
the activities of the alimentary tract, I had occasion to note that
the sensation of hunger was not constant but recurrent, and that
the moment of its disappearance was often associated with a rather
loud gurgling sound as heard through the stethoscope. This and other
evidence, indicative of a source of the hunger sensations in the
contractions of the digestive canal, I reported in 1911.[171] That
same year, with the help of one of my students, A. L. Washburn, I
obtained final proof for this inference.
Appetite and Hunger
The sensations of appetite and hunger are so complex and so
intimately interrelated that any discussion of either sensation is
sure to go astray unless at the start there is clear understanding
of the meanings of the terms. The view has been propounded that
appetite is the first degree of hunger, the mild and pleasant stage,
agreeable in character; and that hunger itself is a more advanced
condition, disagreeable and even painful--the unpleasant result
of not satisfying the appetite.[172] On this basis appetite and
hunger would differ only quantitatively. Another view, which seems
more justifiable, is that the two experiences are fundamentally
different.
Careful observation indicates that appetite is related to previous
sensations of taste and smell of food. Delightful or disgusting
tastes and odors, associated with this or that edible substance,
determine the appetite. It has, therefore, important psychic elements
in its composition. Thus, by taking thought, we can anticipate the
odor of a delicious beefsteak or the taste of peaches and cream,
and in that imagination we can find pleasure. In the realization,
direct effects in the senses of taste and smell give still further
delight. As already noted in the first chapter, observations on
experimental animals and on human beings have shown that the
pleasures of both anticipation and realization, by stimulating the
flow of saliva and gastric juice, play a highly significant rôle
in the initiation of digestive processes.
Among prosperous people, supplied with abundance of food, the
appetite seems sufficient to ensure for bodily needs a proper
supply of nutriment. We eat because dinner is announced, because
by eating we avoid unpleasant consequences, and because food is
placed before us in delectable form and with tempting tastes and
odors. Under less easy circumstances, however, the body needs are
supplied through the much stronger and more insistent demands of
hunger.
The sensation of hunger is difficult to describe, but almost
everyone from childhood has felt at times that dull ache or gnawing
pain referred to the lower mid-chest region and the epigastrium,
which may take imperious control of human actions. As Sternberg
has pointed out, hunger may be sufficiently insistent to force the
taking of food which is so distasteful that it not only fails to
rouse appetite, but may even produce nausea. The hungry being gulps
his food with a rush. The pleasures of appetite are not for him--he
wants quantity rather than quality, and he wants it at once.
Hunger and appetite are, therefore, widely different--in
physiological basis, in localization and in psychic elements. Hunger
may be satisfied while the appetite still calls. Who is still hungry
when the tempting dessert is served, and yet are there any who
refuse it, on the plea that they no longer need it? On the other
hand, appetite may be in abeyance while hunger is goading.[173]
What ravenous boy is critical of his food? Do we not all know that
“hunger is the best sauce”? Although the two sensations may thus
exist separately, they nevertheless have the same function of leading
to the intake of food, and they usually appear together. Indeed,
the coöperation of hunger and appetite is probably the reason for
their being so frequently confused.
The Sensation of Hunger
Hunger may be described as having a central core and certain more
or less variable accessories. The peculiar dull ache of hungriness,
referred to the epigastrium, is usually the organism’s first strong
demand for food; and when the initial order is not obeyed, the
sensation is likely to grow into a highly uncomfortable pang or
gnawing, less definitely localized as it becomes more intense.
This may be regarded as the essential feature of hunger. Besides
the dull ache, however, lassitude and drowsiness may appear, or
faintness, or violent headache, or irritability and restlessness
such that continuous effort in ordinary affairs becomes increasingly
difficult. That these states differ much with individuals--headache
in one and faintness in another, for example--indicates that they
do not constitute the central fact of hunger, but are more or less
inconstant accompaniments. The “feeling of emptiness,” which has
been mentioned as an important element of the experience,[174] is
an inference rather than a distinct datum of consciousness, and can
likewise be eliminated from further consideration. The dull pressing
sensation is left, therefore, as the constant characteristic, the
central fact, to be examined in detail.
Hunger can evidently be regarded from the psychological point of
view, and discussed solely on the basis of introspection; or it can
be studied with reference to its antecedents and to the physiological
conditions which accompany it--a consideration which requires the
use of both objective methods and subjective observation. This
psycho-physiological treatment of the subject will be deferred till
the last. Certain theories which have been advanced with regard to
hunger, and which have been given more or less credit, must first
be examined.
Two main theories have been advocated. The first is supported by
contentions that hunger is a general sensation, arising at no special
region of the body, but having a local reference. This theory has
been more widely credited by physiologists and psychologists than
the other. The other is supported by evidence that hunger has a
local source and therefore a local reference. In the course of our
examination of these views we shall have opportunity to consider
some pertinent new observations.
The Theory That Hunger is a General Sensation
The conception that hunger arises from a general condition of the
body rests in turn on the notion that, as the body uses up material,
the blood becomes impoverished. Schiff[175] advocated this notion,
and suggested that poverty of the blood in food substance affects
the tissues in such manner that they demand a new supply. The nerve
cells of the brain share in this general shortage of provisions,
and because of internal changes, give rise to the sensation. Thus
is hunger explained as an experience dependent on the body as a
whole.
Three classes of evidence are cited in support of this view:
1. “Hunger increases as time passes”--a partial statement. The
development of hunger as time passes is a common observation which
quite accords with the assumption that the condition of the body
and the state of the blood are becoming constantly worse, so long
as the need, once established, is not satisfied.
While it is true that with the lapse of time hunger increases as the
supply of body nutriment decreases, this concomitance is not proof
that the sensation arises directly from a serious encroachment on the
store of food materials. If this argument were valid we should expect
hunger to become more and more distressing until death follows from
starvation. There is abundant evidence that the sensation is not thus
intensified; on the contrary, during continued fasting hunger, at
least in some persons, wholly disappears after the first few days.
Luciani,[176] who carefully recorded the experience of the faster
Succi, states that after a certain time the hunger feelings vanish
and do not return. And he tells of two dogs that showed no signs of
hunger after the third or fourth day of fasting; thereafter they
remained quite passive in the presence of food. Tigerstedt,[177]
who also has studied the metabolism of starvation, declares that
although the desire to eat is very great during the first day of
the ordeal, the unpleasant sensations disappear early, and that at
the end of the fast the subject may have to force himself to take
nourishment. The subject, “J. A.,” studied by Tigerstedt and his
co-workers,[178] reported that after the fourth day of fasting, he
had no disagreeable feelings.
Carrington,[179] after examining many persons who, to better their
health, abstained from eating for different periods, records
that “habit-hunger” usually lasts only two or three days and, if
plenty of water is drunk, does not last longer than three days.
Viterbi,[180] a Corsican lawyer condemned to death for political
causes, determined to escape execution by depriving his body of
food and drink. During the eighteen days that he lived he kept
careful notes. On the third day the sensation of hunger departed,
and although thereafter thirst came and went, hunger never returned.
Still further evidence of the same character could be cited, but
enough has already been given to show that after the first few days
of fasting the hunger feelings may wholly cease. On the theory that
hunger is a manifestation of bodily need, are we to suppose that,
in the course of starvation, the body is mysteriously not in need
after the third day, and that therefore the sensation of hunger
disappears? The absurdity of such a view is obvious.
2. “Hunger may be felt though the stomach be full”--a selected
alternative. Instances of duodenal fistula in man have been carefully
studied, which have shown that a modified sensation of hunger
may be felt when the stomach is full. A famous case described by
Busch[181] has been repeatedly used as evidence. His patient, who
lost nutriment through a duodenal fistula, was hungry soon after
eating, and felt satisfied only when the chyme was restored to the
intestine through the distal fistulous opening. As food is absorbed
mainly through the intestinal wall, the inference is direct that
the general bodily state, and not the local conditions of the
alimentary canal, must account for the patient’s feelings.
A full consideration of the evidence from cases of duodenal fistula
cannot so effectively be presented now as later. That in Busch’s
case hunger disappeared while food was being taken is, as we shall
see, quite significant. It may be that the restoration of chyme
to the intestine quieted hunger, not because nutriment was thus
introduced into the body, but because the presence of material
altered the nature of gastro-intestinal activity. The basis for
this suggestion will be given in due course.
3. “Animals may eat eagerly after section of their vagus and
splanchnic nerves”--a fallacious argument. The third support for
the view that hunger has a general origin in the body is derived
from observations on experimental animals. By severance of the vagus
and splanchnic nerves, the lower esophagus, the stomach and the
small intestine can be wholly separated from the central nervous
system. Animals thus operated upon nevertheless eat food placed
before them, and may indeed manifest some eagerness for it.[182]
How is this behavior to be accounted for--when the possibility of
local stimulation has been eliminated--save by assuming a central
origin of the impulse to eat?
The fallacy of this evidence, though repeatedly overlooked, is easily
shown. We have already seen that appetite as well as hunger may lead
to the taking of food. Indeed, the animal with all gastro-intestinal
nerves cut may have the same incentive to eat that a well-fed man
may have, who delights in the pleasurable taste and smell of food
and knows nothing of hunger pangs. Even when the nerves of taste are
cut, as they were in Longet’s experiments,[183] sensations of smell
are still possible, as well as agreeable associations which can be
roused by sight. More than fifty years ago Ludwig[184] pointed out
that, even if all the nerves were severed, psychic reasons could
be given for the taking of food, and yet because animals eat after
one or another set of nerves is eliminated, the conclusion has been
drawn by various writers that the nerves in question are thereby
proved to be not concerned in the sensation of hunger. Evidently,
since hunger is not required for eating, the act of eating is no
testimony whatever that the animal is hungry, and, after the nerves
have been severed, is no proof that hunger is of central origin.
Weakness of the Assumptions Underlying the Theory
That Hunger is a General Sensation
The evidence thus far examined has been shown to afford only shaky
support for the theory that hunger is a general sensation. The
theory, furthermore, is weak in its fundamental assumptions. There
is no clear indication, for example, that the blood undergoes or has
undergone any marked change, chemical or physical, when the first
stages of hunger appear. There is no evidence of any direct chemical
stimulation of the gray matter of the cerebral cortex. Indeed,
attempts to excite the gray matter artificially by chemical agents
have been without results;[185] and even electrical stimulation,
which is effective, must, in order to produce movements, be so
powerful that the movements have been attributed to excitation
of underlying white matter rather than cells in the gray. This
insensitivity of cortical cells to direct stimulation is not at
all favorable to the notion that they are sentinels set to warn
against too great diminution of bodily supplies.
Body Need May Exist Without Hunger
Still further evidence opposed to the theory that hunger results
directly from the using up of organic stores is found in patients
suffering from fever. Metabolism in fever patients is augmented,
body substance is destroyed to such a degree that the weight of
the patient may be greatly reduced, and yet the sensation of hunger
under these conditions of increased need is wholly lacking.
Again, if a person is hungry and takes food, the sensation is
suppressed soon afterwards, long before any considerable amount of
nutriment could be digested and absorbed, and therefore long before
the blood and the general bodily condition, if previously altered,
could be restored to normal.
Furthermore, persons exposed to privation have testified that hunger
can be temporarily suppressed by swallowing indigestible materials.
Certainly scraps of leather and bits of moss, not to mention clay
eaten by the Otomacs, would not materially compensate for large
organic losses. In rebuttal to this argument the comment has been
made that central states as a rule can be readily overwhelmed by
peripheral stimulation, and just as sleep, for example, can be
abolished by bathing the temples, so hunger can be abolished by
irritating the gastric walls.[186] This comment is beside the point,
for it meets the issue by merely assuming as true the condition
under discussion. The absence of hunger during the ravages of fever,
and its quick abolition after food or even indigestible stuff is
swallowed, still further weakens the argument, therefore, that the
sensation arises directly from lack of nutriment in the body.
The Theory That Hunger is of General Origin Does Not
Explain the Quick Onset and the Periodicity
of the Sensation
Many persons have noted that hunger has a sharp onset. A person
may be tramping in the woods or working in the fields, where
fixed attention is not demanded, and without premonition may feel
the abrupt arrival of the characteristic ache. The expression
“grub-struck” is a picturesque description of this experience. If
this sudden arrival of the sensation corresponds to the general
bodily state, the change in the general bodily state must occur with
like suddenness or have a critical point at which the sensation is
instantly precipitated. There is no evidence whatever that either
of these conditions occurs in the course of metabolism.
Another peculiarity of hunger, which I have already mentioned, is
its intermittency. It may come and go several times in the course
of a few hours. Furthermore, while the sensation is prevailing,
its intensity is not uniform, but marked by ups and downs. In some
instances the ups and downs change to a periodic presence and absence
without change of rate. In my own experience the hunger pangs came
and went on one occasion as follows:
Came Went
12--37--20 38--30
40--45 41--10
41--45 42--25
43--20 43--35
44--40 45--55
46--15 46--30
and so on, for ten minutes longer. Again in this relation, the
intermittent and periodic character of hunger would require, on the
theory under examination, that the bodily supplies be intermittently
and periodically insufficient. During one moment the absence of
hunger would imply an abundance of nutriment in the organism, ten
seconds later the presence of hunger would imply that the stores
had been suddenly reduced, ten seconds later still the absence of
hunger would imply a sudden renewal of plenty. Such zig-zag shifts
of the general bodily state may not be impossible, but from all
that is known of the course of metabolism, such quick changes are
highly improbable. The periodicity of hunger, therefore, is further
evidence against the theory that the sensation has a general basis
in the body.
The Theory That Hunger is of General Origin Does Not
Explain the Local Reference
The last objection to this theory is that it does not account for
the most common feature of hunger--namely, the reference of the
sensation to the region of the stomach. Schiff and others[187]
who have supported the theory have met this objection by two
contentions. First they have pointed out that the sensation is
not always referred to the stomach. Schiff interrogated ignorant
soldiers regarding the local reference; several indicated the neck
or chest, twenty-three the sternum, four were uncertain of any
region, and two only designated the stomach. In other words, the
stomach region was most rarely mentioned.
The second contention against the importance of local reference is
that such evidence is fallacious. An armless man may feel tinglings
which seem to arise in fingers which have long since ceased to be
a portion of his body. The fact that he experiences such tinglings
and ascribes them to dissevered parts, does not prove that the
sensation originates in those parts. And similarly the assignment
of the ache of hunger to any special region of the body does not
demonstrate that the ache arises from that region. Such are the
arguments against a local origin of hunger.
Concerning these arguments we may recall, first, Schiff’s admission
that the soldiers he questioned were too few to give conclusive
evidence. Further, the testimony of most of them that hunger
seemed to originate in the chest or region of the sternum cannot
be claimed as unfavorable to a peripheral source of the sensation.
The description of feelings which develop from disturbances within
the body is almost always indefinite. As Head[188] and others
have shown, conditions in a viscus which give rise to sensation
are likely not to be attributed to the viscus, but to related skin
areas. Under such circumstances we do not dismiss the testimony as
worthless merely because it may not point precisely to the source
of the trouble. On the contrary, we use such testimony constantly
as a basis for judging internal disorders.
With regard to the contention that reference to the periphery is
not proof of the peripheral origin of a sensation, we may answer
that the force of that contention depends on the amount of accessory
evidence which is available. Thus if we see an object come into
contact with a finger, we are justified in assuming that the
simultaneous sensation of touch which we refer to that finger has
resulted from the contact, and is not a purely central experience
accidentally attributed to an outlying member. Similarly in the
case of hunger--all that we need as support for the peripheral
reference of the sensation is proof that conditions occur there,
simultaneously with hunger pangs, which might reasonably be regarded
as giving rise to those pangs.
With the requirement in mind that peripheral conditions be adequate,
let us examine the state of the fasting stomach to see whether,
indeed, conditions may be present in times of hunger which would
sustain the theory that hunger has a local outlying source.
Hunger Not Due To Emptiness of the Stomach
Among the suggestions which have been offered to account for a
peripheral origin of the sensation is that of attributing it to
emptiness of the stomach. By use of the stomach tube Nicolai[189]
found that when his subjects had their first intimation of hunger
the stomach was quite empty. But, in other instances, after lavage
of the stomach, the sensation did not appear for intervals varying
between one and a half and three and a half hours. During these
intervals the stomach must have been empty, and yet no sensation
was experienced. The same testimony was given long before by
Beaumont,[190] who, from his observations on Alexis St. Martin,
declared that hunger arises some time after the stomach is normally
evacuated. Mere emptiness of the organ, therefore, does not explain
the phenomenon.
Hunger Not Due to Hydrochloric Acid in the Empty Stomach
A second theory, apparently suggested by observations on cases
of hyperacidity, is that the ache or pang is due to the natural
hydrochloric acid of the stomach but secreted while the organ is
empty. Again the facts are hostile. Nicolai[191] reported that the
gastric wash-water from his hungry subjects was neutral or only
slightly acid. This testimony confirms Beaumont’s statement, and
is in complete agreement with the results of gastric examination
of fasting animals reported by numerous experimenters. There is no
secretion into the empty stomach during the first days of starvation.
Furthermore, persons suffering from absence of hydrochloric acid
(achylia gastrica) declare that they have normal feelings of hunger.
Hydrochloric acid cannot, therefore, be called upon to account for
the sensation.
Hunger Not Due to Turgescence of the
Gastric Mucous Membrane
Another theory, which was first advanced by Beaumont,[192] is
that hunger arises from turgescence of the gastric glands. The
disappearance of the pangs as fasting continues has been accounted
for by supposing that the gastric glands share in the general
depletion of the body, and that thus the turgescence is relieved.[*]
This turgescence theory has commended itself to several recent
writers. Thus Luciani[193] has accepted it, and by adding the idea
that nerves distributed to the mucosa are specially sensitive
to deprivation of food he accounts for the hunger pangs. Also
Valenti[194] declared a few years ago that the turgescence theory
of Beaumont is the only one with a semblance of truth in it. The
experimental work reported by these two investigators, however, does
not necessarily sustain the turgescence theory. Luciani severed
the previously exposed vagi after cocainizing them, and Valenti
merely cocainized the nerves; the fasting dogs, eager to eat a few
minutes previous to this operation, now ran about as before, but
when offered food, licked and smelled it, but did not take it.
This total neglect of the food lasted varying periods up to two
hours. The vagus nerves seem, indeed, to convey impulses which
affect the procedure of eating, but there is no clear evidence
that those impulses arise from distention of the gland cells. The
turgescence theory, moreover, does not explain the effect of taking
indigestible material into the stomach. According to Pawlow, and to
others who have observed human beings, the chewing and swallowing of
unappetizing stuff does not cause any secretion of gastric juice (see
p. 8). Yet such stuff when swallowed will cause the disappearance
of hunger, and Nicolai found that the sensation could be abolished
by simply introducing a stomach sound. It is highly improbable that
the turgescence of the gastric glands can be reduced by either of
these procedures. The turgescence theory, furthermore, does not
explain the quick onset of hunger, or its intermittent and periodic
character. That the cells are repeatedly swollen and contracted
within periods a few seconds in duration is almost inconceivable.
For these reasons, therefore, the theory that hunger results from
turgescence of the gastric mucosa can reasonably be rejected.
*[Footnote: A better explanation perhaps is afforded by Boldireff’s
discovery that at the end of two or three days the stomachs of
fasting dogs begin to secrete gastric juice and continue the
secretion indefinitely. (Boldireff, Archives Biologiques de St.
Petersburg, 1905, xi, p. 98.)]
Hunger the Result of Contractions
There remain to be considered, as a possible cause of hunger pangs,
contractions of the stomach and other parts of the alimentary
canal. This suggestion is not new. Sixty-nine years ago Weber[195]
declared his belief that “strong contraction of the muscle fibres
of the wholly empty stomach, whereby its cavity disappears, makes
a part of the sensation which we call hunger.” Vierordt[196] drew
the same inference twenty-five years later (in 1871), and since
then Ewald, Knapp, and Hertz have declared their adherence to this
view. These writers have not brought forward any direct evidence for
their conclusion, though Hertz has cited Boldireff’s observations on
fasting dogs as probably accounting for what he terms “the gastric
constituent of the sensation.”
The Empty Stomach and Intestine Contract
The argument commonly used against the gastric contraction theory
is that the stomach is not energetically active when empty. Thus
Schiff[197] stated, “The movements of the empty stomach are rare
and much less energetic than during digestion.” Luciani[198]
expressed his disbelief by asserting that gastric movements are
much more active during gastric digestion than at other times, and
cease almost entirely when the stomach has discharged its contents.
And Valenti[199] stated (1910), “We know very well that gastric
movements are exaggerated while digestion is proceeding in the
stomach, but when the organ is empty they are more rare and much
less pronounced,” and, therefore, they cannot account for hunger.
Evidence opposed to these suppositions has been in existence
for many years. In 1899 Bettmann[200] called attention to the
contracted condition of the stomach after several days’ fast. In
1902 Wolff[201] reported that after forty-eight hours without food
the stomach of the cat may be so small as to look like a slightly
enlarged duodenum. In a similar circumstance I have noticed the same
extraordinary smallness of the organ, especially in the pyloric
half. The anatomist His[202] also recorded his observation of the
phenomenon. In 1905 Boldireff[203] demonstrated that the whole
gastro-intestinal tract has a periodic activity while not digesting.
Each period of activity lasts from twenty to thirty minutes, and
is characterized in the stomach by rhythmic contractions ten to
twenty in number. These contractions, Boldireff reports, may be
stronger than during digestion, and his published records clearly
support this statement. The intervals of repose between periodic
recurrences of the contractions lasted from one and a half to two
and a half hours. Especially noteworthy is Boldireff’s observation
that if fasting is continued for two or three days, the groups of
contractions appear at gradually longer intervals and last for
gradually shorter periods, and thereupon, as the gastric glands
begin continuous secretion, all movements cease.
Observations Suggesting that Contractions Cause Hunger
The research, previously mentioned, on the rhythmic sounds produced
by the digestive process, I was engaged in when Boldireff’s paper
was published. That contractions of the alimentary canal on a
gaseous content might explain the hunger pangs which I had noticed
seemed probable at that time, especially in the light of Boldireff’s
observations. Indeed, Boldireff[204] himself had considered hunger
in relation to the activities he described, but solely with the idea
that hunger might _provoke_ them; and since the activities dwindled
in force and frequency as time passed, whereas, in his belief, they
should have become more pronounced, he abandoned the notion of any
relation between the phenomena. Did not Boldireff misinterpret
his own observations? When he was considering whether hunger might
cause the contractions, did he not overlook the possibility that
the contractions might cause hunger? A number of experiences have
led to the conviction that Boldireff did, indeed, fail to perceive
part of the significance of his results. For example, I have noticed
the disappearance of a hunger pang as gas was heard gurgling upward
through the cardia. That the gas was rising rather than being forced
downward was proved by its regurgitation immediately after the sound
was heard. In all probability the pressure that forced the gas from
the stomach was the cause of the preceding sensation of hunger.
Again the sensation can be momentarily abolished a few seconds
after swallowing a small accumulation of saliva or a teaspoonful
of water. If the stomach is in strong contraction in hunger, this
result can be accounted for, in accordance with the observations of
Lieb and myself,[205] as due to the inhibition of the contraction
by swallowing. Thus also could be explained the prompt vanishing of
the ache soon after we begin to eat, for repeated swallowing results
in continued inhibition.[*] Furthermore, Ducceschi’s discovery[206]
that hydrochloric acid diminishes the tonus of the pyloric portion
of the stomach may have its application here; the acid would be
secreted as food is taken and would then cause relaxation of the
very region which is most strongly contracted.
*[Footnote: The absence of hunger in Busch’s patient while food
was being eaten (see p. 239) can also be accounted for in this
manner.]
The Concomitance of Contractions and Hunger in Man
Although the evidence above outlined had led me to the conviction
that hunger results from contractions of the alimentary canal, direct
proof was still lacking. In order to learn whether such proof might
be secured, Washburn determined to become accustomed to the presence
of a rubber tube in the esophagus.[*] Almost every day for several
weeks Washburn introduced as far as the stomach a small tube, to
the lower end of which was attached a soft-rubber balloon about
8 centimeters in diameter. The tube was thus carried about each
time for two or three hours. After this preliminary experience the
introduction of the tube and its presence in the gullet and stomach
were not at all disturbing. When a record was to be taken, the
balloon, placed just within the stomach, was moderately distended
with air, and was connected with a water manometer ending in a
cylindrical chamber 3.5 centimeters wide. A float recorder resting
on the water in the chamber permitted registering any contractions
of the fundus of the stomach. On the days of observation Washburn
would abstain from breakfast, or eat sparingly; and without taking
any luncheon would appear in the laboratory about two o’clock. The
recording apparatus was arranged as above described. In order to
avoid any error that might arise from artificial pressure on the
balloon, a pneumograph, fastened below the ribs, was made to record
the movements of the abdominal wall. Uniformity of these movements
would show that no special contractions of the abdominal muscles
were made. Between the records of gastric pressure and abdominal
movement, time was marked in minutes, and an electromagnetic signal
traced a line which could be altered by pressing a key. All these
recording arrangements were out of Washburn’s sight; he sat with
one hand at the key, ready whenever the sensation of hunger was
experienced to make the current which moved the signal.
*[Footnote: Nicolai (_loc. cit._) reported that although the
introduction of a stomach tube at first abolished hunger in his
subjects, with repeated use the effects became insignificant.]
Sometimes the observations were started before any hunger was noted;
at other times the sensation, after running a course, gave way to a
feeling of fatigue. Under either of these circumstances there were
no contractions of the stomach. When Washburn stated that he was
hungry, however, powerful contractions of the stomach were invariably
being registered. As in my own earlier experience, the sensations
were characterized by periodic recurrences with free intervals,
or by periodic accesses of an uninterrupted ache. The record of
Washburn’s introspection of his hunger pangs agreed closely with
the record of his gastric contractions. Almost invariably, however,
the contraction nearly reached its maximum before the record of
the sensation was started (see Fig. 37).
[Illustration: Figure 37.--One-half the original size. The top
record represents intragastric pressure (the small oscillations
due to respiration, the large to contractions of the stomach); the
second record is time in minutes (ten minutes); the third record
is W’s report of hunger pangs; the lowest record is respiration
registered by means of a pneumograph about the abdomen.]
This fact may be regarded as evidence that the contraction precedes
the sensation, and not _vice versa_, as Boldireff considered it.
The contractions were about a half-minute in duration, and the
intervals between varied from thirty to ninety seconds, with an
average of about one minute. The augmentations of intragastric
pressure in Washburn ranged between eleven and thirteen in twenty
minutes; I had previously counted in myself eleven hunger pangs in
the same time. The rate in each of us was, therefore, approximately
the same. This rate is slightly slower than that found in dogs by
Boldireff; the difference is perhaps correlated with the slower
rhythm of gastric peristalsis in man compared with that in the
dog.[207]
Before hunger was experienced by Washburn the recording apparatus
revealed no signs of gastric activity. Sometimes a rather tedious
period of waiting had to be endured before contractions occurred.
And after they began they continued for a while, then ceased (see
Fig. 38). The feeling of hunger, which was reported while the
contractions were recurring, disappeared as the waves stopped. The
inability of the subject to control the contractions eliminated
the possibility of their being artifacts, perhaps induced by
suggestion. The close concomitance of the contractions with hunger
pangs, therefore, clearly indicates that they are the real source
of those pangs.
[Illustration: Figure 38.--One-half the original size. The same
conditions as in Fig. 37. (Fifteen minutes.) There was a long
wait for hunger to disappear. After x, W. reported himself “tired
but not hungry.” The record from y to z was the continuance, on
a second drum, of x to y.]
Boldireff’s studies proved that when the empty stomach is manifesting
periodic contractions, the intestines also are active. Conceivably
all parts of the alimentary canal composed of smooth muscle share
in these movements. The lower esophagus in man is provided with
smooth muscle. It was possible to determine whether this region in
Washburn was active during hunger.
To the esophageal tube a thin-rubber finger-cot (2 centimeters
in length) was attached and lowered into the stomach. The little
rubber bag was distended with air, and the tube, pinched to keep the
bag inflated, was gently withdrawn until resistance was felt. The
air was now released from the bag and the tube farther withdrawn
about 3 centimeters. The bag was again distended with air at a
manometric pressure of 10 centimeters of water. Inspiration now
caused the writing lever, which recorded the pressure changes, to
rise; and a slightly farther withdrawal of the tube changed the
rise, on inspiration, to a fall. The former position of the tube,
therefore, was above the gastric cavity and below the diaphragm. In
this position the bag, attached to a float recorder (with chamber
2.3 centimeters in diameter), registered the periodic oscillations
shown in Fig. 39. Though individually more prolonged than those of
the stomach, these contractions, it will be noted, occur at about
the same rate.
[Illustration: Figure 39.--One-half the original size. The top
record represents compression of thin rubber bag in the lower
esophagus. The pressure in the bag varied between 9 and 13
centimeters of water. The cylinder of the recorder was of smaller
diameter than that used in the gastric records. The esophageal
contractions compressed the bag so completely that, at the summits
of the large oscillations, the respirations were not registered.
When the oscillations dropped to the time line, the bag was about
half inflated. The middle line registers time in minutes (ten
minutes). The bottom record is W’s report of hunger pangs.]
This study of hunger, reported by Washburn and myself in 1912, has
since been taken up by Carlson of Chicago, and in observations
on a man with a permanent gastric fistula, as well as on himself
and his collaborators, he has fully confirmed our evidence as to
the relation between contractions of the alimentary canal and the
hunger sensation. In a series of nearly a score of interesting
papers, Carlson and his students[208] have greatly amplified our
knowledge of the physiology of the “empty” stomach. Not only are
there the contractions observed by Washburn and myself, but at times
these may fuse into a continuous cramp of the gastric muscle. The
characteristic contractions, furthermore, continue after the vagus
nerve supply to the stomach has been destroyed, and, therefore, are
not dependent on the reception of impulses by way of the cranial
autonomic fibres. Recently Luckhardt and Carlson have brought
forward evidence that the blood of a fasting animal if injected into
the vein of a normal animal is capable of inducing in the latter
the condition of cramp or tetanus in the gastric muscle mentioned
above--an effect which does not occur when the blood of a well-fed
animal is injected. It seems _possible_ that a substance exists in
the blood which acts to excite the gastric hunger mechanism. But
this point will require further investigation.
With these demonstrations that contractions are the immediate cause
of hunger, most of the difficulties confronting other explanations
are readily obviated. Thus the sudden onset of hunger and its
peculiar periodicity--phenomena which no other explanation of hunger
can account for--are at once explained.
In fever, when bodily material is being most rapidly used, hunger
is absent. Its absence is understood from an observation made
by F. T. Murphy and myself,[209] that infection, with systemic
involvement, is accompanied by a total cessation of all movements
of the alimentary canal. Boldireff observed that when his dogs were
fatigued the rhythmic contractions failed to appear. Being “too
tired to eat” is thereby given a rational explanation.
A pathological form of the sensation--the inordinate hunger
(bulimia) of certain neurotics--is in accordance with the well-known
disturbances of the tonic innervation of the alimentary canal in
such individuals.
Since the lower end of the esophagus, as well as the stomach,
contracts periodically in hunger, the reference of the sensation
to the sternum by the ignorant persons questioned by Schiff was
wholly natural. The activity of the lower esophagus also explains
why, after the stomach has been removed, or in some cases when the
stomach is distended with food, hunger can still be experienced.
Conceivably the intestines also originate vague sensations by their
contractions. Indeed, the final banishment of the modified hunger
sensation in the patient with duodenal fistula, described by Busch,
may have been due to the lessened activity of the intestines when
chyme was injected into them.
The observations recorded in this paper have, as already noted,
numerous points of similarity to Boldireff’s observations[210] on
the periodic activity of the alimentary canal in fasting dogs.
Each period of activity, he found, comprised not only widespread
contractions of the digestive canal, but also the pouring out of
bile, and of pancreatic and intestinal juices rich in ferments.
Gastric juice was not secreted at these times; when it was secreted
and reached the intestine, the periodic activity ceased. What is
the significance of this extensive disturbance? I have elsewhere
presented evidence[211] that gastric peristalsis is dependent on the
stretching of gastric muscle when tonically contracted. The evidence
that the stomach is in fact strongly contracted in hunger--i. e.,
in a state of high tonus--has been presented above.[*] Thus the
very condition which causes hunger and leads to the taking of food
is the condition, when the swallowed food stretches the shortened
muscles, for immediate starting of gastric peristalsis. In this
connection the observations of Haudek and Stigler[212] are probably
significant. They found that the stomach discharges its contents more
rapidly if food is eaten in hunger than if not so eaten. Hunger, in
other words, is normally the signal that the stomach is contracted
for action; the unpleasantness of hunger leads to eating; eating
starts gastric digestion, and abolishes the sensation. Meanwhile
the pancreatic and intestinal juices, as well as bile, have been
prepared in the duodenum to receive the oncoming chyme. The periodic
activity of the alimentary canal in fasting, therefore, is not solely
the source of hunger pangs, but is at the same time an exhibition
in the digestive organs of readiness for prompt attack on the food
swallowed by the hungry animal.
*[Footnote: The “empty” stomach and esophagus contain gas (see
Hertz: Quarterly Journal of Medicine, 1910, iii, p. 378; Mikulicz:
Mittheilungen aus den Grenzgebieten der Medicin und Chirurgie,
1903, xii, p. 596). They would naturally manifest rhythmic
contractions on shortening tonically on their content.]
REFERENCES
[Footnote 171: Cannon: The Mechanical Factors of Digestion, London
and New York, 1911, p. 204.]
[Footnote 172: Bardier: Richet’s Dictionnaire de Physiologie, article
Faim, 1904, vi, p. 1. See, also, Howell: Text-book of Physiology,
fourth edition, Philadelphia and London, 1911, p. 285.]
[Footnote 173: See Sternberg: Zentralblatt für Physiologie, 1909,
xxii, p. 653. Similar views were expressed by Bayle in a thesis
presented to the Faculty of Medicine in Paris in 1816.]
[Footnote 174: See Hertz: The Sensibility of the Alimentary Canal,
London, 1911, p. 38.]
[Footnote 175: Schiff: Physiologie de la Digestion, Florence and
Turin, 1867, p. 40.]
[Footnote 176: Luciani: Das Hungern, Hamburg and Leipzig, 1890, p.
113.]
[Footnote 177: Tigerstedt: Nagel’s Handbuch der Physiologie, Berlin,
1909, i, p. 376.]
[Footnote 178: Johanson, Landergren, Sonden and Tigerstedt:
Skandinavisches Archiv für Physiologie, 1897, vii, p. 33.]
[Footnote 179: Carrington: Vitality, Fasting and Nutrition, New
York, 1908, p. 555.]
[Footnote 180: Viterbi, quoted by Bardier: _Loc. cit._, p. 7.]
[Footnote 181: Busch: Archiv für pathologische Anatomie und
Physiologie und für klinische Medicin, 1858, xiv, p. 147.]
[Footnote 182: See Schiff: _Loc. cit._, p. 37; also Ducceschi;
Archivio di Fisiologia, 1910, viii, p. 579.]
[Footnote 183: Longet: Traité de Physiologie, Paris, 1868, i, p.
23.]
[Footnote 184: Ludwig: Lehrbuch der Physiologie des Menschen,
Leipzig and Heidelberg, 1858, ii, p. 584.]
[Footnote 185: Maxwell: Journal of Biological Chemistry, 1906-7,
ii, p. 194.]
[Footnote 186: See Schiff: _Loc. cit._, p. 49.]
[Footnote 187: See Schiff: _Loc. cit._, p. 31; Bardier; _Loc. cit._,
p. 16.]
[Footnote 188: Head: Brain, 1893, xvi, p. 1; 1901, xxiv, p. 345.]
[Footnote 189: Nicolai: Ueber die Entstehung des Hungergefühls,
Inaugural Dissertation, Berlin, 1892, p. 17.]
[Footnote 190: Beaumont: The Physiology of Digestion, second edition,
Burlington, 1847, p. 51.]
[Footnote 191: Nicolai: _Loc. cit._, p. 15.]
[Footnote 192: Beaumont: _Loc. cit._, p. 55.]
[Footnote 193: Luciani: Archivio di Fisiologia, 1906, iii, p. 54.
Tiedemann long ago suggested that gastric nerves become increasingly
sensitive as fasting progresses. (Physiologie des Menschen,
Darmstadt, 1836, iii, p. 22.)]
[Footnote 194: Valenti: Archives Italiennes de Biologie, 1910,
liii, p. 94.]
[Footnote 195: Weber: Wagner’s Handwörterbuch der Physiologie,
1846, iii², p. 580.]
[Footnote 196: Vierordt: Grundriss der Physiologie, Tübingen, 1871,
p. 433.]
[Footnote 197: Schiff: _Loc. cit._, p. 33.]
[Footnote 198: Luciani: _Loc. cit._, p. 542.]
[Footnote 199: Valenti: _Loc. cit._, p. 95.]
[Footnote 200: Bettmann: Philadelphia Monthly Medical Journal,
1899, i, p. 133.]
[Footnote 201: Wolff: Dissertation, Giessen, 1902, p. 9.]
[Footnote 202: His: Archiv für Anatomie, 1903, p. 345.]
[Footnote 203: Boldireff: _Loc. cit._, p. 1.]
[Footnote 204: Boldireff: _Loc. cit._, p. 96.]
[Footnote 205: See Cannon and Lieb: American Journal of Physiology,
1911, xxix, p. 267.]
[Footnote 206: Ducceschi: Archivio per le Scienze Mediche, 197,
xxi, p. 154.]
[Footnote 207: See Cannon: American Journal of Physiology, 1903,
viii, p. xxi; 1905, xiv, p. 344.]
[Footnote 208: See American Journal of Physiology, 1913, 1914.]
[Footnote 209: Cannon and Murphy: Journal of the American Medical
Association, 1907, xlix, p. 840.]
[Footnote 210: Boldireff: _Loc. cit._, pp. 108-111.]
[Footnote 211: Cannon: American Journal of Physiology, 1911, xxix,
p. 250.]
[Footnote 212: Haudek and Stigler: Archiv für die gesammte
Physiologie, 1910, cxxxiii, p. 159.]
CHAPTER XIV
THE INTERRELATIONS OF EMOTIONS
Emotions gain expression through discharges along the neurones of
the autonomic nervous system. The reader will recall that this
system has three divisions--the cranial and sacral, separated by
the sympathetic--and that when the neurones of the mid-division
meet in any organ the neurones of either of the end divisions, the
influence of the two sets is antagonistic. As previously stated (p.
35), there is evidence that arrangements exist in the central nervous
system for reciprocal innervation of these antagonistic divisions,
just as there is reciprocal innervation of antagonistic skeletal
muscles. The characteristic affective states manifested in the
working of these three divisions have been described. Undoubtedly,
these states have correspondents--activities and inhibitions--in
the central neurones. The question now arises, are the states which
appear in opposed divisions also in opposition?
Antagonism Between Emotions Expressed in the Sympathetic
and in the Cranial Divisions of the Autonomic System
The cranial autonomic, as already shown, is concerned with the quiet
service of building up reserves and fortifying the body against
times of stress. Accompanying these functions are the relatively
mild pleasures of sight and taste and smell of food. The possibility
of existence of these gentle delights of eating and drinking and
also of their physiological consequences is instantly abolished in
the presence of emotions which activate the sympathetic division.
The secretion of saliva, gastric juice, pancreatic juice and bile
is stopped, and the motions of the stomach and intestines cease at
once, both in man and in the lower animals, whenever pain, fear,
rage, or other strong excitement is present in the organism.
All these disturbances of digestion seem mere interruptions of
the “normal” course of events unless the part they may play in
adaptive reactions is considered. In discussing the operations of
the sympathetic division, I pointed out that all the bodily changes
which occur in the intense emotional states--such as fear and
fury--occur as results of activity in this division, and are in the
highest degree serviceable in the struggle for existence likely to
be precipitated when these emotions are aroused. From this point
of view these perturbations, which so readily seize and dominate
the organs that in quiet times are commonly controlled by the
cranial autonomic, are bodily reactions which may be of the utmost
importance to life at times of critical emergency. Thus are the
body’s reserves--the stored adrenin and the accumulated sugar--called
forth for instant service; thus is the blood shifted to nerves and
muscles that may have to bear the brunt of struggle; thus is the
heart set rapidly beating to speed the circulation; and thus, also,
are the activities of the digestive organs for the time abolished.
Just as in war between nations the arts and industries which have
brought wealth and contentment must suffer serious neglect or be
wholly set aside both by the attacker and the attacked, and all
the supplies and energies developed in the period of peace must be
devoted to the present conflict; so, likewise, the functions which
in quiet times establish and support the bodily reserves are, in
times of stress, instantly checked or completely stopped, and these
reserves lavishly drawn upon to increase power in the attack and
in the defense or flight.[*]
*[Footnote: One who permits fears, worries and anxieties to
disturb the digestive processes when there is nothing to be done,
is evidently allowing the body to go onto what we may regard as
a “war footing,” when there is no “war” to be waged, no fighting
or struggle to be engaged in.]
It is, therefore, the natural antagonism between these two processes
in the body--between saving and expenditure, between preparation and
use, between anabolism and catabolism--and the correlated antagonism
of central innervations, that underlie the antipathy between the
emotional states which normally accompany the processes. The desire
for food, the relish of eating it, all the pleasures of the table,
are naught in the presence of anger or great anxiety. And of the
two sorts of emotional states, those which manifest themselves
in the dominant division of the autonomic hold the field also in
consciousness.
Antagonism Between Emotions Expressed in the Sympathetic
and in the Sacral Divisions of the Autonomic System
The nervi erigentes are the part of the sacral autonomic in which
the peculiar excitements of sex are expressed. As previously
stated, these nerves are opposed by branches from the sympathetic
division--the division which is operated characteristically in the
major emotions.
The opposition in normal individuals between the emotional states
which appear in these two antagonistic divisions is most striking.
Even in animals as low in the scale as birds, copulation is not
performed “until every condition of circumstance and sentiment is
fulfilled, until time, place and partner all are fit.”[213] And
among men the effect of fear or momentary anxiety or any intense
emotional interest in causing inhibition of the act can be supported
by cases in the experience of any physician with extensive practice.
Indeed, as Prince[214] has stated, “the suppression of the sexual
instinct by conflict is one of the most notorious experiences
of this kind in everyday life. This instinct cannot be excited
during an attack of fear or anger, and even during moments of its
excitation, if there is an invasion of another strong emotion the
sexual instinct at once is repressed. Under these conditions, as
with other instincts, even habitual excitants can no longer initiate
the instinctive process.”
When the acme of excitement is approaching it is probable that the
sympathetic division is also called into activity; indeed, the
completion of the process--the contractions of the seminal vesicles
and the prostate, and the subsidence of engorged tissues, all
innervated by sympathetic filaments (see pp. 32, 33)--may be due
to the overwhelming of sacral by sympathetic nervous discharges.
As soon as this stage is reached the original feeling likewise has
been dissipated.
The other parts of the sacral division which supply the bladder
and rectum are so nearly free from any emotional tone in their
normal reflex functioning that it is unnecessary to consider them
further with reference to emotional antagonisms. Mild affective
states, such as worry and anxiety, can, to be sure, check the
activity of the colon and thus cause constipation.[215] But the
augmented activity of these parts (contraction of the bladder and
rectum) in very intense periods of emotional stress, when the
sympathetic division is strongly innervated, presents a problem of
some difficulty. Possibly in such conditions the orderliness of the
central arrangements is upset, just as it is after tetanus toxin or
strychnine poisoning, and opposed innervations no longer discharge
reciprocally, but simultaneously, and then the stronger member of
the pair prevails. Only on such a basis, at present, can I offer
any explanation for the activity and the supremacy of the sacral
innervation of the bladder and distal colon when the sympathetic
innervation is aroused, as, for example, in great fright.
The Function of Hunger
A summary in few words of the chief functions typically performed
or supported by each division of the autonomic would designate
the cranial division as the upbuilder and restorer of the organic
reserves, the sacral as the servant of racial continuity, and the
sympathetic as the preserver of the individual. Self-preservation
is primary and essential; on that depends racial continuity, and
for that all the resources of the organism are called forth.
Analogously the sympathetic innervations, when they meet in organs
innervated also by the cranial and sacral divisions, almost without
exception predominate over their opponents. And analogously, also,
the emotional states which are manifested in the sympathetic
division and are characteristically much more intense than those
manifested in the other divisions, readily assume ascendancy also
in consciousness.
It is obvious that extended action of the sympathetic division,
abolishing those influences of the cranial division which are
favorable to proper digestion and nutrition, might defeat its own
ends. Interruption of the nutritional process for the sake of
self-preservation through defense or attack can be only temporary;
if the interruption were prolonged, there might be serious danger to
the vigor of the organism from failure to replenish the exhausted
stores. The body does not have to depend on the return of a banished
appetite, however, before its need for restoration is attended
to. There is a secondary and very insistent manner in which the
requirement of food is expressed, and that is through the repeated
demands of hunger.
Unlike many other rhythmically repeated sensations, hunger is not
one that anybody becomes accustomed to and neglects because of its
monotony. During the period of his confinement in the citadel of
Magdeburg, the celebrated political adventurer Baron von Trenck[216]
was allowed only a pound and a half of ammunition bread and a jug
of water as his daily ration. “It is impossible for me to describe
to my reader,” he wrote in his memoirs, “the excess of tortures
that during eleven months I endured from ravenous hunger. I could
easily have devoured six pounds of bread every day; and every
twenty-four hours, after having received and swallowed my small
portion, I continued as hungry as before I began, yet I was obliged
to wait another twenty-four hours for a new morsel.... My tortures
prevented sleep, and looking into futurity, the cruelty of my fate
seemed to me, if possible, to increase, for I imagined that the
prolongation of pangs like these was insupportable. God preserve
every honest man from sufferings like mine! They were not to be
endured by the most obdurate villain. Many have fasted three days,
many have suffered want for a week or more, but certainly no one
besides myself ever endured it in the same excess for eleven months;
some have supposed that to eat little might become habitual, but I
have experienced the contrary. My hunger increased every day, and
of all the trials of fortitude my whole life has afforded, this
eleven months was the most bitter.”[*]
*[Footnote: In all probability the continued experience of hunger
pangs reported by Baron von Trenck was due to the repeated eating
of amounts of food too small to satisfy the bodily demand. The
reader will recall that persons who for some time take no food
whatever report that the disagreeable feelings are less intense
or disappear after the third or fourth day (see p. 238).]
Thus, although the taking of food may be set in abeyance at times
of great excitement, and the bodily reserves fully mobilized, that
phase of the organism’s self-protecting adjustment is limited,
and then hunger asserts itself as an agency imperiously demanding
restoration of the depleted stores.
The Similarity of Visceral Effects in Different
Strong Emotions and Suggestions as to its
Psychological Significance
The dominant emotions which we have been considering as
characteristically expressed in the sympathetic division of the
autonomic system are fear and rage. These two emotions are not
unlike. As James[217] has indicated, “Fear is a reaction aroused by
the same objects that arouse ferocity.... We both fear and wish to
kill anything that may kill us; and the question which of the two
impulses we shall follow is usually decided by some one of those
_collateral circumstances_ of the particular case, to be moved by
which is the mark of superior mental natures.” The cornering of an
animal when in the headlong flight of fear may suddenly turn the
fear to fury and the flight to a fighting in which all the strength
of desperation is displayed.
Furthermore, these dominant emotions are states into which many
other commonly milder affective states may be suddenly transformed.
As McDougall[218] has pointed out, all instinctive impulses when
met with opposition or obstruction give place to, or are complicated
by, the pugnacious or combative impulse directed against the source
of the obstruction. A dog will bristle at any attempt to take away
his food, males will fight furiously when provoked by interference
with the satisfaction of the sexual impulse, a man will forget
the conventions and turn hot for combat when there is imputation
against his honor, and a mother all gentle with maternal devotion
is stung to quick resentment and will make a fierce display of her
combative resources, if anyone intentionally injures her child.
In these instances of thwarted or disturbed instinctive acts the
emotional accompaniments--such as the satisfaction of food and of
sexual affection, the feeling of self-pride, and the tender love
of a parent--are whirled suddenly into anger. And anger in one is
likely to provoke anger or fear in the other who for the moment
is the object of the strong feeling of antagonism. Anger is the
emotion preëminently serviceable for the display of power, and fear
is often its counterpart.
The visceral changes which accompany fear and rage are the result of
discharges by way of sympathetic neurones. It will be recalled that
these neurones are arranged for diffuse rather than for narrowly
directed effects. So far as these two quite different emotions are
concerned, present physiological evidence indicates that differences
in visceral accompaniments[*] are not noteworthy--for example,
either fear or rage stops gastric secretion (see pp. 10, 11). There
is, indeed, obvious reason why the visceral changes in fear and
rage should not be _different_, but rather, why they should be
_alike_. As already pointed out, these emotions accompany organic
preparations for action, and just because the conditions which
evoke them are likely to result in flight or conflict (either one
requiring perhaps the utmost struggle), the bodily needs in either
response are precisely the same.
*[Footnote: Obvious vascular differences, as pallor or flushing
of the face, are of little significance. With increase of blood
pressure from vasoconstriction, pallor might result from action
of the constrictors in the face, or flushing might result because
constrictors elsewhere, as, for example, in the abdomen, raised
the pressure so high that facial constrictors are overcome. Such,
apparently, is the effect of adrenin already described (see
p. 107). Or the flushing might occur from local vasodilation.
That very different emotional states may have the same vascular
accompaniments was noted by Darwin (The Expression of Emotions
in Man and Animals, New York, 1905), who mentioned the pallor of
rage (p. 74) and also of terror (p. 77).]
In discussing the functioning of the sympathetic division I pointed
out that it was roused to activity not only in fear and rage, but
also in pain. The machinery of this division likewise is operated
wholly or partially in emotions which are usually mild--such as joy
and sorrow and disgust--_when they become sufficiently intense_.
Thus, for instance, the normal course of digestion may be stopped
or quite reversed in a variety of these emotional states.
Darwin[219] reports the case of a young man who on hearing that a
fortune had just been left him, became pale, then exhilarated, and
after various expressions of joyous feeling vomited the half-digested
contents of his stomach. Müller[220] has described the case of a
young woman whose lover had broken the engagement of marriage.
She wept in bitter sorrow for several days, and during that time
vomited whatever food she took. And Burton,[221] in his _Anatomy of
Melancholy_, gives the following instance of the effect of disgust:
“A gentlewoman of the same city saw a fat hog cut up, when the
entrails were opened, and a noisome savour offended her nose, she
much misliked, and would not longer abide; a physician in presence
told her, as that hog, so was she, full of filthy excrements, and
aggravated the matter by some other loathsome instances, insomuch
this nice gentlewoman apprehended it so deeply that she fell
forthwith a vomiting, was so mightily distempered in mind and body,
that with all his art and persuasion, for some months after, he
could not restore her to herself again, she could not forget or
remove the object out of her sight.”
In these three cases, of intense joy, intense sorrow and intense
disgust, the influence of the cranial division of the autonomic
has been overcome, digestion has ceased, and the stagnant gastric
contents by reflexes in striated muscles have been violently
discharged. The extent to which under such circumstances other
effects of sympathetic impulses may be manifested, has not, so far
as I know, been ascertained.
From the evidence just given it appears that any high degree of
excitement in the central nervous system, whether felt as anger,
terror, pain, anxiety, joy, grief or deep disgust, is likely to
break over the threshold of the sympathetic division and disturb
the functions of all the organs which that division innervates. It
may be that there is advantage in the readiness with which these
widely different emotional conditions can express themselves in this
one division, for, as has been shown (see p. 276), occasions may
arise when these milder emotions are suddenly transmuted into the
naturally intense types (as fright and fury) which normally activate
this division; and if the less intense can also influence it, the
physiological aspect of the transmutation is already partially
accomplished.
If various strong emotions can thus be expressed in the diffused
activities of a single division of the autonomic--the division
which accelerates the heart, inhibits the movements of the stomach
and intestines, contracts the blood vessels, erects the hairs,
liberates sugar, and discharges adrenin--it would appear that the
bodily conditions which have been assumed, by some psychologists, to
distinguish emotions from one another must be sought for elsewhere
than in the viscera. We do not “feel sorry because we cry,” as James
contended, but we cry because when we are sorry or overjoyed or
violently angry or full of tender affection--when any one of these
diverse emotional states is present--there are nervous discharges
by sympathetic channels to various viscera, including the lachrymal
glands. In terror and rage and intense elation, for example, the
responses in the viscera seem too uniform to offer a satisfactory
means of distinguishing states which, in man at least, are very
different in subjective quality. For this reason I am inclined to
urge that the visceral changes merely contribute to an emotional
complex more or less indefinite, but still pertinent, feelings of
disturbance in organs of which we are not usually conscious.
This view that the differential features of emotions are not to be
traced to the viscera is in accord with the experimental results of
Sherrington,[222] who has demonstrated that emotional responses occur
in dogs in which practically all the main viscera and the great bulk
of skeletal muscle have been removed from subjection to and from
influence upon the brain, by severance of the vagus nerves and the
spinal cord. In these animals no alteration whatever was noticed in
the occurrence, under appropriate circumstances, of characteristic
expressions of voice and features, indicating anger, delight or
fear. The argument that these expressions may have been previously
established by afferent impulses from excited viscera was met by
noting that a puppy only nine weeks old also continued to exhibit
the signs of emotional excitement after the brain was disconnected
from all the body except the head and shoulders. Evidence from
uniformity of visceral response and evidence from exclusion of the
viscera are harmonious, therefore, in minimizing visceral factors
as the source of differences in emotional states.[*]
*[Footnote: The paucity of afferent fibres in the autonomic system,
and the probability of an extremely low degree of sensitiveness
in the viscera (for evidence, see Cannon: The Mechanical Factors
of Digestion, London, 1911, p. 202), likewise support this
conclusion.]
If these differences are due to other than visceral changes, why
is it not always possible by voluntary innervations to produce
emotions? We can laugh and cry and tremble. But forced laughter does
not bring happiness, nor forced sobbing sorrow, and the trembling
from cold rouses neither anger nor fear. The muscle positions and
tensions are there, but the experiencing of such bodily changes does
not seem even approximately to rouse an emotion in us. Voluntary
assumption of an attitude seems to leave out the “feeling.” It
is probable, however, that no attitude which we can assume has
all the elements in it which appear in the complete response to a
stirring situation. But is not this because the natural response is
a _pattern reaction_, like inborn reflexes of low order, such as
sneezing, in which impulses flash through peculiarly coöperating
neurone groups of the central system, suddenly, unexpectedly, and in
a manner not exactly reproducible by volition, and thus they throw
the skeletal muscles into peculiar attitudes and, if sufficiently
intense, rush out in diffuse discharges that cause tremors and
visceral perturbations? The typical facial and bodily expressions,
automatically assumed in different emotions, indicate the discharge
of peculiar groupings of neurones in the several affective states.
That these responses occur instantly and spontaneously when the
appropriate “situation,” actual or vividly imagined, is present,
shows that they are ingrained in the nervous organization. At
least one such pattern, that of anger, persists after removal of
the cerebral hemispheres--the decorticated dog, by growling and
biting when handled, has the appearance of being enraged;[223] the
decerebrate cat, when vigorously stimulated, retracts its lips and
tongue, stares with dilated pupils, snarls and snaps its jaws.[224]
On the other hand, stroking the hair, whistling and gently calling
to produce a pleased attitude, or yelling to produce fright, have
not the slightest effect in evoking from the decorticated dog signs
of joy and affection or of fear, nor does the animal manifest any
sexual feeling. The absence of bodily indications of these emotions
is quite as significant as the presence of the signs of anger.
For since expressions of anger can persist without the cerebral
cortex, there is little reason why the complexes of other emotional
expressions, if their “machinery” exists below the cortex, should
not also be elicitable. That they are not elicitable suggests that
they require a more elaborately organized grouping of neurones than
does anger--possibly what the cortex, or the cortex in combination
with basal ganglia, would provide.
The contrast between the brevity of the “pseudo-affective reactions”
in the decerebrate cat, though the viscera are still connected with
the central nervous system, and the normal duration of emotional
expression in the dog with the body separated from the head region,
has been used by Sherrington to weigh the importance of the visceral
and other factors. And the evidence which I have given above, as
well as that which he has offered, favors the view that the viscera
are relatively unimportant in an emotional complex, especially in
contributing differential features.
REFERENCES
[Footnote 213: James: Principles of Psychology, New York, 1905, i,
p. 22.]
[Footnote 214: Prince: The Unconscious, New York, 1914, p. 456.]
[Footnote 215: Hertz: Constipation and Allied Intestinal Disorders,
London, 1909, p. 81.]
[Footnote 216: v. Trenck: Merkwürdige Lebensgeschichte, Berlin,
1787, p. 195.]
[Footnote 217: James, _Loc. cit._, p. 415.]
[Footnote 218: McDougall: Introduction to Social Psychology, London,
1908, p. 72.]
[Footnote 219: Darwin: _Loc. cit._, p. 76.]
[Footnote 220: Müller: Deutsches Archiv für klinische Medicin,
1907, lxxxix, p. 434.]
[Footnote 221: Burton: The Anatomy of Melancholy (first published
in 1621), London, 1886, p. 443.]
[Footnote 222: Sherrington: Proceedings of the Royal Society, 1900,
lxvi, p. 397.]
[Footnote 223: Goltz: Archiv für die gesammte Physiologie, 1892,
li, p. 577.]
[Footnote 224: Woodworth and Sherrington: Journal of Physiology,
1904, xxxi, p. 234.]
CHAPTER XV
ALTERNATIVE SATISFACTIONS FOR THE FIGHTING EMOTIONS
The uniformity of visceral responses when almost any feelings grow
very intense, and under such conditions the identity of these
responses with those characteristically aroused in the belligerent
emotion of anger or rage and its counterpart, fear, offer interesting
possibilities of transformation and substitution. This is especially
true in the activities of human beings. And because men have devised
such terribly ingenious and destructive modes of expressing these
feelings in war, an inquiry into the basis for possible substitution
seems not out of place.
Support for the Militarist Estimate of the Strength of
the Fighting Emotions and Instincts
The business of killing and of avoiding death has been one of the
primary interests of living beings throughout their long history
on the earth. It is in the highest degree natural that feelings
of hostility often burn with fierce intensity, and then, with
astonishing suddenness, that all the powers of the body are called
into action--for the strength of the feelings and the quickness of
the response measure the chances of survival in a struggle where
the issue may be life or death. These are the powerful emotions
and the deeply ingrained instinctive reactions which invariably
precede combat. They are the emotions and instincts that sometimes
seize upon individuals in groups and spread like wildfire into
larger and larger aggregations of men, until vast populations are
shouting and clamoring for war. To whatever extent military plans
are successful in devising a vast machine for attack or defense, the
energies that make the machine go are found, in the last analysis,
in human beings who, when the time for action comes, are animated
by these surging elemental tendencies which assume control of their
conduct and send them madly into conflict.
The strength of the fighting instinct in man has been one of the
main arguments used by the militarists in support of preparation for
international strife. They point to the historical fact that even
among highly civilized peoples scarcely a decade passes without a
kindling of the martial emotions, which explode in actual warfare.
Such fighting, they say, is inevitable--the manifestation of
“biological law”--and, so long as human nature remains unchanged,
decision by battle must be resorted to. They urge, furthermore,
that in war and in the preparations for war important physical
qualities--sturdiness, hardihood, and strength for valorous
deeds--are given peculiarly favorable opportunities for development,
and that if these opportunities are lacking, lusty youth will give
place to weaklings and mollycoddles. In addition the militarists
say that war benefits mankind by its moral effects. Without war
nations become effete, their ideals become tarnished, the people
sink into self-indulgence, their wills weaken and soften in luxury.
War, on the contrary, disciplines character, it sobers men, it
teaches them to be brave and patient, it renews a true order of
values, and its demand for the supreme sacrifice of life brings
forth in thousands an eager response that is the crowning glory of
the human spirit. As the inevitable expression of a deep-rooted
instinct, therefore, and as a unique means of developing desirable
physical and moral qualities, war is claimed by the militarists to
be a natural necessity.[225]
The militarist contention that the fighting instinct is firmly fixed
in human nature receives strong confirmation in the results of our
researches. Survival has been decided by the grim law of mortal
conflict, and the mechanism for rendering the body more competent in
conflict has been revealed in earlier chapters as extraordinarily
perfect and complete. Moreover, the physiological provisions for
fierce struggle are found not only in the bodies of lower animals,
that must hunt and kill in order to live, but also in human beings.
Since this remarkable mechanism is present, and through countless
generations has served the fundamentally important purpose of giving
momentous aid in the struggle for existence, the militarists might
properly argue that, as with other physiological processes, bodily
harmony would be promoted by its exercise. Indeed, they might account
for the periodic outburst of belligerent feelings by assuming that
these natural aptitudes require occasional satisfaction.[*]
*[Footnote: Mr. Graham Wallas has made the interesting suggestion
(The Great Society, New York, 1914, p. 66) that nervous strain
and restlessness due to “baulked disposition” may result from the
absence of circumstances which would call the emotional responses
into action. And he cites Aristotle’s theory that pent passions
may be released by represented tragedy and by music.]
Growing Opposition to the Fighting Emotions and
Instincts as Displayed in War
In spite of the teachings of history that wars have not grown fewer,
and in spite of the militarist argument that war is a means of
purging mankind of its sordid vices, and renewing instead the noblest
virtues, the conclusion that the resort to arms is unavoidable and
desirable is nowadays being strongly contested. The militarists show
only part of the picture. No large acquaintance with the character
of warfare is necessary to prove that when elemental anger, hate
and fear prevail, civilized conventions are abandoned and the most
savage instincts determine conduct. Homes are looted and burned,
women and children are abominably treated, and many innocents are
murdered outright or starved to death. No bland argument for the
preservation of the manly virtues can palliate such barbarities.
Even when fighting men are held within the rules, the devices for
killing and injuring are now made so perfect by devilish ingenuity
that by the pulling of a trigger one man can in a few seconds mow
down scores of his fellow-creatures and send them writhing to agony
or death. War has become too horrible; it is conducted on too
stupendous a scale of carnage and expenditure; it destroys too many
of the treasured achievements of the race; it interferes too greatly
with consecrated efforts to benefit all mankind by discovery and
invention; it involves too much suffering among peoples not directly
concerned in the struggle; it is too vastly at variance with the
methods of fair dealing that have been established between man and
man; the human family has become too closely knit to allow some of
its members to bring upon themselves and all the rest poverty and
distress and a long heritage of bitter hatred and resolution to
seek revenge.
All these reasons for hostility to war imply a thwarting of strong
desires in men--desires for family happiness, devotion to beauty
and to scholarship, passion for social justice, hopes of lessening
poverty and disease. As was pointed out in the previous chapter,
the feeling of hostility has no definite object to awaken it. It is
roused when there is opposition to what we ardently wish to get.
And because war brings conditions which frustrate many kinds of
eagerly sought purposes, war has roused in men a hostility against
itself. There is then a war against war, a willingness to fight
against monstrous carnage and destruction, that grows in intensity
with every war that is waged.
The Desirability of Preserving the Martial Virtues
Although there is increasing opposition to the display of the
fighting emotions and instincts in war, nevertheless the admirable
moral and physical qualities, claimed by the militarists to be
the unique products of war, are too valuable to be lost. As
McDougall[226] has indicated, when the life of ideas becomes richer,
and the means we take to overcome obstructions to our efforts more
refined and complex, the instinct to fight ceases to express itself
in its crude natural manner, save when most intensely excited, and
becomes rather a source of increased energy of action towards the end
set by any other instinct; the energy of its impulses adds itself
to and reënforces that of other impulses and so helps us to overcome
our difficulties. In this lies its great value for civilized man. A
man devoid of the pugnacious instinct would not only be incapable
of anger, but would lack this great source of reserve energy which
is called into play in most of us by any difficulty in our path.
Thus the very efficiency of a war against war, as well as struggle
against other evils that beset civilized society, rests on the
preservation and use of aggressive feeling and the instinct to
attack. From this point of view the insistence by the militarists
that we must accept human nature as we find it, and that the attempt
to change it is foolish, seems a more justifiable attitude than
that of the pacifists who belittle the fighting qualities and urge
that changing them is a relatively simple process. We should not
wish them changed. Even if in the war against war a means should
be established of securing international justice, and if through
coöperative action the decrees of justice were enforced, so that
the occasions which would arouse belligerent emotions and instincts
were much reduced, there would still remain the need of recognizing
their elemental character and their possible usefulness to society.
What is needed is not a suppression of these capacities to feel and
act, but their diversion into other channels where they may have
satisfactory expression.
Moral Substitutes for Warfare
“We must make new energies and hardihoods continue the manliness
to which the military mind so faithfully clings. Martial virtues
must be the enduring cement; intrepidity, contempt of softness,
surrender of private interest, obedience to command, must still
remain the rock upon which states are built.” Thus wrote William
James[227] in proposing a “moral equivalent for war.” This, he
suggested, should consist of such required service in the hard
and difficult occupations as would take the childishness and
superciliousness out of our youth and give them soberer ideas and
healthier sympathies with their fellow-men. He conceived that by
proper direction of its education a people should become as proud
of the attainment by the nation of superiority in any ideal respect
as it would be if the nation were victorious in war. “The martial
type of character,” he declared, “can be bred without war. Strenuous
honor and disinterestedness abound elsewhere. Priests and medical
men are in a fashion educated to it, and we should all feel some
degree of it imperative if we were conscious of our work as an
obligatory service to the state. We should be _owned_, as soldiers
are by the army, and our pride would rise accordingly. We could
be poor, then, without humiliation, as army officers now are. The
only thing needed henceforth is to inflame the civic temper as
past history has inflamed the military temper.”
Similar ideas have been expressed by others.[228] It has been pointed
out that the great war of mankind is that against pain, disease,
poverty and sin; that the real heroes are not those who squander
human strength and courage in fighting one another, but those who
fight for man against these his eternal foes. War of man against
man, in this view, becomes dissension in the ranks, permitting the
common enemies to strike their most telling blows.
These moral considerations, however, are apart from the main intent
of our discussion. Our earlier inquiry confirmed the belief that the
fighting emotions are firmly rooted in our natures, and showed that
these emotions are intimately associated with provisions for physical
exertion. It is particularly in this aspect of the discussion of
substitutes for war that these studies have significance.
Physical Substitutes for Warfare
The idealization of the state and the devotion of service to social
welfare, which have been suggested as moral substitutes for military
loyalty, leave unanswered the claims of the militarists that in
war and in preparations for war opportunities are offered which
are peculiarly favorable to the development of important physical
qualities--bodily vigor, sturdiness, and ability to withstand all
manner of hardships.
In the evidence previously presented, it seems to me there was a
suggestion that offers a pertinent alternative to these claims.
When the body goes onto what we have called a war footing, the
physiological changes that suddenly occur are all adapted to the
putting forth of supreme muscular and nervous efforts. That was
what primitive battle consisted of, through countless myriads of
generations--a fierce physical contest of beast with beast, and of
man with man. Such contests, attended as they were by the thrill
of unpredictable incidents, and satisfying completely the lust of
combat, are to be contrasted with the dull grind in preparation
for modern war, the monotonous regularity of subservience, the
substitution everywhere of mechanism for muscle, and often the
attack on an enemy who lies wholly unseen.[*] As Wallas with nice
irony has remarked, “The gods in Valhalla would hardly choose the
organization of modern lines of military communication, as they chose
the play of sword and spear, to be the most exquisite employment
of eternity.”
*[Footnote: Lord Wolseley, while commander-in-chief of the English
forces, in 1897, secured sanction for not displaying the regimental
colors in battle. “It would be madness and a crime,” he declared,
“to order any soldier to carry colors into action in the future.
You might quite as well order him to be assassinated. We have
had most reluctantly to abandon a practice to which we attached
great importance, and which, under past and gone conditions of
fighting, was invaluable in keeping alive the regimental spirit
upon which our British troops depended so much.” All war has been
transformed by the invention of the far-reaching and fate-dealing
rifle and automatic gun, with which an enemy kills, whose face is
not even seen. War is almost reduced to a mechanical interchange
of volleys and salvoes, and to the intermittent fire of rifles
and machine guns, with short rushes at the last, in which there
is no place for the dignity and grace of the antique battle of
the standard. (See London Times, July 31, 1897, p. 12.)
T. F. Millard, the well-known correspondent of the Russo-Japanese
War, wrote as follows of the characteristics of present day
conflicts: “A large part of modern war is on too great a scale
to give much opportunity for individual initiative. Soldiers can
rarely tell what is going on in their immediate vicinity. They
cannot always see the enemy they are firing at, and where they can
see the object of their fire such an important matter as range
and even direction cannot be left to them.... Troops are clothed
so much alike nowadays that it is very difficult to distinguish
friend from foe at five hundred yards, and large bodies of troops
rarely get that close to each other in modern war while there is
light enough to see clearly.... Battery officers simply see that
their guns are handled according to instructions. They regulate
the time, speed, objective and range as ordered.... The effects
of the fire are observed by officers appointed to that duty,
stationed at various parts of the field, often miles and miles
apart, and who are in constant communication with the chief of
artillery by telephone.” (See Scribner’s Magazine, 1905, xxxvii,
pp. 64, 66.)
The testimony of a captain of a German battery engaged against
the French and English in 1914, supports the foregoing claims.
He is reported as saying: “We shoot over those tree tops yonder
in accordance with directions for range and distance which come
from somewhere else over a field telephone, but we never see the
men at whom we are firing. They fire back without seeing us, and
sometimes their shells fall short or go beyond us, and sometimes
they fall among us and kill and wound a few of us. Thus it goes
on day after day. I have not with my own eyes seen a Frenchman
or an Englishman unless he was a prisoner. It is not so much
pleasure--fighting like this.” (See Philadelphia Saturday Evening
Post, December 26, 1914, p. 27.)]
While it is true that physical strength can be developed by any
form of hard labor, as, for example, by sawing wood or digging
ditches, such labor does not stimulate quickness, alertness, and
resourcefulness in bodily action. Nor does it give any occasion for
use of the emotional mechanism for reënforcement. If this mechanism,
like other physiological arrangements, is present in the body for
use--and previous discussion leaves little doubt of that--then as
a means of exercising it and, in addition, satisfying the strong
instinct for competitive testing of strength and physical skill,
some activity more enlivening than monotonous gymnastics and ordered
marching is required.
In many respects strenuous athletic rivalries present, better than
modern military service, the conditions for which the militarists
argue, the conditions for which the body spontaneously prepares
when the passion for fighting prevails. As explained in an
earlier chapter, in competitive sports the elemental factors are
retained--man is again pitted against man, and all the resources
of the body are summoned in the eager struggle for victory. And
because, under such circumstances, the same physiological alterations
occur that occur in anticipation of mortal combat, the belligerent
emotions and instincts, so far as their bodily manifestations are
concerned, are thereby given complete satisfaction.
The Significance of International Athletic Competitions
For reasons given above, I venture to lay emphasis on a suggestion,
which has been made before by others, that the promotion of great
international athletic contests, such as the Olympic games, would
do for our young men much that is now claimed as peculiar to the
values of military discipline. The substitution of athletic rivalries
for battle is not unknown. In the Philippine Islands, according
to Worcester,[229] there were no athletics before the American
occupation. The natives soon learned games from the soldiers. And
when the sports reached such development that competition between
towns and provinces was possible, they began to arouse the liveliest
enthusiasm among the people. The physical development of the
participants has been greatly stimulated, the spirit of fair play
and sportsmanship, formerly lacking, has sprung into existence in
every section of the Islands, and the annual meets between athletic
teams from various provinces are recognized as promoting a general
and friendly understanding among the different Filipino tribes. The
fierce Igarots of Bontoc, once constantly at war with neighboring
tribes, now show their prowess not in head-hunting, but in baseball,
wrestling, and the tug-of-war.[*]
*[Footnote: It is reported that when these warriors first appeared
at the games, each brought his spear, which he drove into the
ground beside him, ready for use. As the nature of the new
rivalries became known, the spears were left behind.]
Is it unreasonable to expect that what has happened in the Philippine
Islands might, by proper education and suggestion, happen elsewhere
in the world? Certainly the interest in athletic contests is no
slight and transient interest. At the time of a great war we know
that news of the games is fully as much demanded as news of the
war. Already in the United States, without special stimulation, the
number of young men engaged in athletic training is estimated as
equal to the number in the standing army. And in England, belief
in the efficacy of athletics as a means of promoting hardihood
and readiness to face stern hazards has found expression in the
phrase that England’s battles have been won on the football fields
of Rugby and of Eton. With the further promotion of international
contests the influence of competitive sports is likely to increase
rather than lessen. Within national boundaries emulation is sure
to stimulate extensively such games as will bring forth the best
representative athletes that the country can produce. In one of
the high-spirited European nations, which made a poor showing at
the last Olympic meet, thousands of young men began training for
the next meet, under a director imported from the nation that had
made the highest records.
Training for athletic contests is quite as likely to enure young
men to physical hardship and fatigue, is quite as conducive to
the development of bodily vigor, the attainment of alertness and
skill and the practice of self-restraint, as is army life with its
traditional associations and easy license. It may be urged, however,
that an essential element is lacking in all this discussion--the
sobering possibility that in war the supreme surrender of life itself
may be required. Death for one’s country is indeed glorious. But the
argument that being killed is desirable has little to commend it.
When the strongest and sturdiest are constantly chosen to be fed to
the engines of annihilation, the race is more likely to lose greater
values than it gains from the spectacle of self-sacrifice, however
perfect that may be. Are there not advantages in the conditions of
great athletic rivalries that may compensate for war’s most austere
demand? The race of hardy men, to secure which the militarists urge
war, is much more likely to result from the honoring and preserving
of vigorous men in their vigor than it is from the systematic
selection of such men to be destroyed in their youth.
There are other aspects of international games which strongly commend
them as an alternative to the pursuit of military discipline.
The high standards of honor and fairness in sport; its unfailing
revelation of excellence without distinctions of class, wealth,
race or color; the ease with which it becomes an expression of
the natural feelings of patriotism; the respect which victory and
pluckily borne defeat inspire in competitors and spectators alike;
the extension of acquaintance and understanding which follows from
friendly and magnanimous rivalry among strong men who come together
from the ends of the earth--each of these admirable features of
athletic contests between nations might be enlarged upon. But, as
intimated before, these moral considerations must be left without
further mention, as being irrelevant to the physiological processes
with which we are dealing.
We are concerned with the question of exercising the fighting
instinct and thus assuring the physical welfare of the race. The
race must degenerate, the militarists say, if this instinct is not
allowed to express itself in war. This declaration we are in a
position to deny, for the evidence is perfectly clean-cut that the
aggressive instincts, which through æons of racial experience have
naturally and spontaneously developed vigor and resourcefulness in
the body, are invited by elemental emotions, and that through these
emotions energies are released which are highly useful to great
physical effort. No stupid routine of drill, or any other deadening
procedure, will call these energizing mechanisms into activity. War
and the preparations for war nowadays have become too machine-like
to serve as the best means of preserving and disciplining these
forces. The exhilarating swing and tug and quick thrust of the big
limb muscles have largely vanished. Pressing an electric contact or
bending the trigger finger is a movement altogether too trifling.
If, then, natural feelings must be expressed, if the fighting
functions of the body must be exercised, how much better that these
satisfactions be found in natural rather than in artificial actions,
how much more reasonable that men should struggle for victory in
the ancient ways, one against another, body and spirit, as in the
great games.
REFERENCES
[Footnote 225: See Angell: The Great Illusion, New York and London,
1913, pp. 159-164.]
[Footnote 226: McDougall: Introduction to Social Psychology, London,
1908, p. 61.]
[Footnote 227: James: Memories and Studies, New York, 1911, p. 287.]
[Footnote 228: See Perry: The Moral Economy, New York, 1909, p.
32; and Drake: Problems of Conduct, Boston, 1914, p. 317.]
[Footnote 229: Worcester: The Philippines, Past and Present, New
York, 1914, ii, pp. 515, 578.]
A LIST OF PUBLISHED RESEARCHES FROM THE PHYSIOLOGICAL
LABORATORY IN HARVARD UNIVERSITY, ON WHICH THE PRESENT
ACCOUNT IS BASED.
1. The Influence of Emotional States on the Functions of the
Alimentary Canal. By W. B. Cannon. American Journal of the Medical
Sciences, 1909, cxxxvii, pp. 480-487.
2. Emotional Stimulation of Adrenal Secretion. By W. B. Cannon and
D. de la Paz. American Journal of Physiology, 1911, xxviii, pp.
64-70.
3. The Effects of Asphyxia, Hyperpnœa, and Sensory Stimulation on
Adrenal Secretion. By W. B. Cannon and R. G. Hoskins. _Ibid._,
1911, xxix, pp. 274-279.
4. Emotional Glycosuria. By W. B. Cannon, A. T. Shohl and W. S.
Wright. _Ibid._, 1911, xxix, pp. 280-287.
5. A Consideration of Some Biological Tests for Epinephrin. By R.
G. Hoskins. Journal of Pharmacology and Experimental Therapeutics,
1911, iii, pp. 93-99.
6. The Sthenic Effect of Epinephrin upon Intestine. By R. G. Hoskins.
American Journal of Physiology, 1912, xxix, pp. 363-366.
7. An Explanation of Hunger. By W. B. Cannon and A. L. Washburn.
_Ibid._, 1912, xxix, pp. 441-454.
8. A New Colorimetric Method for the Determination of Epinephrin.
By O. Folin, W. B. Cannon and W. Denis. Journal of Biological
Chemistry, 1913, xiii, pp. 477-483.
9. The Depressor Effect of Adrenalin on Arterial Pressure. By W.
B. Cannon and Henry Lyman. American Journal of Physiology, 1913,
xxxi, pp. 376-398.
10. The Effect of Adrenal Secretion on Muscular Fatigue. By W. B.
Cannon and L. B. Nice. _Ibid._, 1913, xxxii, pp. 44-60.
11. Fatigue as Affected by Changes of Arterial Pressure. By C. M.
Gruber. _Ibid._, 1913, xxxii, pp. 222-229.
12. The Threshold Stimulus as Affected by Fatigue and Subsequent
Rest. By C. M. Gruber. _Ibid._, 1913, xxxii, pp. 438-449.
13. The Fatigue Threshold as Affected by Adrenalin and by Increased
Arterial Pressure. By C. M. Gruber. _Ibid._, 1914, xxxiii, pp.
335-355.
14. The Emergency Function of the Adrenal Medulla in Pain and the
Major Emotions. By W. B. Cannon. _Ibid._, 1914, xxxiii, pp. 356-372.
15. The Relation of Adrenalin to Curare and Fatigue in Normal and
Denervated Muscles. By C. M. Gruber. _Ibid._, 1914, xxxiv, pp.
89-96.
16. The Graphic Method of Recording Coagulation. By W. B. Cannon
and W. L. Mendenhall. _Ibid._, 1914, xxxiv, pp. 225-231.
17. The Hastening or Retarding of Coagulation by Adrenalin
Injections. By W. B. Cannon and Horace Gray. _Ibid._, 1914, xxxiv,
pp. 232-242.
18. The Hastening of Coagulation by Stimulating the Splanchnic
Nerves. By W. B. Cannon and W. L. Mendenhall. _Ibid._, 1914, xxxiv,
pp. 243-250.
19. The Hastening of Coagulation in Pain and Emotional Excitement.
By W. B. Cannon and W. L. Mendenhall. _Ibid._, 1914, xxxiv, pp.
251-261.
20. The Interrelations of Emotions as Suggested by Recent
Physiological Researches. By W. B. Cannon. American Journal of
Psychology, 1914, xxv, pp. 256-282.
INDEX
Adrenal extract: effect of, on muscular contraction, 82.
Adrenal glands: nerve supply of, 37;
stimulated in emotion, 52-59, 62-63;
stimulated in pain, 59-62, 63;
in relation to blood sugar, 77;
removal of, causes muscular weakness, 81;
secretion of, improves contraction of fatigued muscle, 92;
variations in adrenin content of, 171;
latent period of, when splanchnics stimulated, 188;
amount of secretion from, when splanchnics stimulated, 198;
fatigue of, 199;
stimulated by asphyxia, 206-208.
Adrenin: secreted by adrenal glands, 36;
action of, identical with sympathetic impulses, 37, 64;
secretion of, by splanchnic stimulation, 41-43;
secreted in emotional excitement, 44, 52-59;
method of testing for, in blood, 47-50;
secreted in emotion, 52-59, 62-63;
disappearance of, from blood, 58;
secreted in pain, 59-62, 63;
effects of, when injected into body, 64-65;
effect of, on distribution of blood in the body, 107;
quickly restores fatigued muscle to normal irritability, 119-123;
specific in its restorative action, 124-128;
as an antidote to muscular metabolites, 129;
restores fatigued denervated muscle to normal irritability,
130;
point of action of, in muscle, 128-133;
antagonistic to curare, 132;
induces rapid coagulation of blood, 136, 147 ff.;
not the direct cause of rapid coagulation, 156-158;
fails to shorten coagulation time in absence of intestines and
liver, 157-158;
variable amount of, in adrenal glands, 171;
emergency functions of, 185 ff.;
utility of, in bettering the contraction of fatigued muscle,
194-195;
not a check to use of sugar in the body, 197, 199;
amount of, secreted when splanchnics stimulated, 198;
a condition for increase of blood sugar, 199;
stimulates the heart, 191, 201;
dilates the bronchioles, 204;
secretion of, increased in asphyxia, 206-208.
Amyl nitrite: effect of, on contraction of fatigued muscle, 126.
Anger: associated with action, 188;
energizing influence of, 216.
Antagonisms: autonomic, 34;
in relation to emotions, 38;
between cranial and sympathetic divisions, 268-270;
between sacral and sympathetic divisions, 270-272.
Appetite: compared with hunger, 233, 235;
operation of, after section of vagus and splanchnic nerves,
240.
Arterial blood pressure: increased in excitement, 95;
artificial methods of increasing, 97;
influence of different heights of, on fatigue, 97-102;
influence of increase of, on fatigue, 97-102;
influence of decrease of, on fatigue, 102-104;
the “critical region” in decreasing, 104;
explanation of effects on fatigued muscle, of varying, 104-106;
value of increased, in pain and emotion, 106.
Arteries: innervation of, 26.
Asphyxia: increases adrenal secretion, 206-208;
increases sugar in blood, 209.
Athletes: glycosuria of, after games, 75.
Autonomic nervous system: three divisions of, 25;
arrangement of sympathetic division of, 26-29;
arrangement of cranial and sacral divisions of, 29-30;
general functions of cranial division of, 30-32;
general functions of sacral division of, 32-34;
antagonism between sympathetic and cranial-sacral divisions
of, 34-36;
identity of action of sympathetic division of, and adrenal
secretion, 36-38;
antagonisms between emotions expressed in, 268-272.
Behavior: biological explanation of, 2.
Bile: flow of, inhibited by excitement, 13.
Bladder: innervation of, 27, 32;
effects of emotions on, 33.
Blood: method of obtaining, for test for adrenin, 45-46;
method of testing, for adrenin, 47-50;
sugar in, 66, 73-74;
distribution of, as affected by adrenin, pain and excitement,
107-108, 200;
functions of, 135;
rapid coagulation of, by adrenin, 136 ff.;
drawing of, for testing coagulation time, 140-142;
treatment of, in testing coagulation time, 142-145;
faster coagulation of, after subcutaneous injections of adrenin,
147-150,
and after intravenous injections, 150-156;
oscillations in the rate of coagulation of, 155;
rapid coagulation of, not due directly to adrenin, 156-158;
rapid coagulation of, not caused by adrenin in absence of liver
and intestines, 157-158,
and not caused by increase of blood sugar, 159, 170;
coagulation of, hastened by splanchnic stimulation, 162-167,
but not in absence of adrenal glands, 167-171;
possible delay of coagulation of, after stimulation of hepatic
nerves, 170;
coagulation of, hastened by “painful” stimulation, 172-177;
coagulation of, hastened in light anesthesia, 174-177;
rapid coagulation of, after excitement, stopped by severing
splanchnic nerves, 180-182;
utility of increased sugar in, 188-193;
distribution of, in pain and excitement, favorable to muscular
effort, 201;
sugar in, increased by asphyxia, 209;
utility of rapid coagulation of, 211.
Bronchioles: dilated by adrenin, 204.
Bulimia: explanation of, 262.
Coagulation, see Blood.
Coagulometer: graphic, 138-147.
Combat: relation of emotion and endurance in, 225-226;
nature of ancient, 294.
Constipation: as result of worry and anxiety, 271.
Cortex, cerebral: insensitiveness of, 242.
Cranial autonomic division: functions of, to conserve bodily
resources, 30-32, 268;
activities of, suppressed by activities of sympathetic division,
268-272.
Curare: action of, antagonized by adrenin, 132.
Dances: relation of excitement and endurance in, 222-224.
Danger: stimulating effect of, 230.
Dervishes: exhibitions of endurance by, 224.
Digestion: interruption of, by strong emotion, 9-12, 13-18,
268-269.
Emotions: surface signs of, 3;
favorable to digestive secretions, 4-8;
unfavorable to digestive secretions, 9-13;
persistence of effects of, on digestive secretions, 12;
effects of, on gastric and intestinal contractions, 13-18;
in relation to sympathetic division, 36;
in relation to adrenal secretion, 44, 52-59, 62-63;
increase of blood sugar in, 66, 73;
glycosuria in, 70-76;
influence of, on distribution of blood in body, 108;
faster coagulation of blood in, 177-182,
but stopped by cutting splanchnics, 180-182;
value of forced respiration in, 203;
value of bronchiolar dilation in, 204;
relation to action, 215;
displayed in a “pattern” response, 218, 282;
in relation to exhibitions of power and endurance, 215, 229;
antagonisms between cranial and sympathetic, 268-270,
and between sacral and sympathetic, 270-272;
similarity of visceral changes in strong, 275-279;
dependence of, on cerebral cortex, 282-283.
Endurance: feats of, related to great emotion, 217-218;
in the excitements of mania and dancing, 222-224;
stimulated by music, 228.
Esophagus: contractions of, associated with hunger sensation,
259-260.
Fatigue: of muscle, 84;
muscular, lessened by splanchnic stimulation, 89-93;
as affected by increase of arterial pressure, 97-102;
irritability of muscle in, increased by splanchnic stimulation,
101;
explanation of effects of varied arterial pressure on, 104-106;
lessens neuro-muscular irritability, 114-117, 120;
effect of, on curarized muscle, 132;
utility of adrenin in lessening effects of, 194, 195;
of adrenal glands, 199;
cessation of hunger contractions in, 262.
Fear: anticipatory character of, 186-187;
associated with action, 188;
explanation of paralyzing effect of, 189;
energizing influence of, 216;
relation to rage, 275;
bodily changes in, like those in rage, 276-277;
importance of, as a fighting emotion, 286.
“Fesselungsdiabetes,” 69.
Fever: absence of hunger in, 242, 263.
Fighting emotions: bodily changes in, like those in competitive
sports, 219-221, 296;
anger and fear as, 285;
importance of, 286;
satisfactions for, in competitive sports, 301.
Food: effect of sight and smell of, on gastric secretion, 6.
Football: glycosuria in players of, 75;
relation of excitement and power in, 219-221.
Frenzy: endurance in, 223, 224.
Ganglia: autonomic, 23.
Gastric glands: turgescence of, not the cause of hunger sensation,
249-250.
Gastric juice: psychic secretion of, 5-8, 11;
importance of, for intestinal digestion, 7;
flow of, inhibited by excitement, 9-12,
and by pain, 19.
Generative organs: innervation of, 32, 33;
effects of strong emotions on activities in, 271.
Glycosuria: in pain, 69-70;
in emotion, 70-76;
after football, 75, 221;
after examinations, 76;
dependence of, on adrenal glands, 77.
Heart: innervation of, 26, 31;
use of sugar by, 191;
stimulated by adrenin, 191, 201.
Hunger: compared with appetite, 233, 235;
description of, 234-236;
theories of, 237;
as a general sensation, 237;
disappearance of, as time passes, 238-239;
when stomach full, 239;
may be absent in bodily need, 242-243;
temporarily abolished by indigestible materials, 243;
quick onset and periodicity of, 244-245;
reference of, to stomach region, 245-247;
not due to emptiness of stomach, 248;
not due to hydrochloric acid in empty stomach, 248;
not due to turgid gastric glands, 249-250;
as the result of contractions, 251-253;
inhibited by swallowing, 254;
method of recording gastric contractions in, 255-256;
associated with gastric contractions, 256-259,
and with esophageal contractions, 259-260;
function of, 263-264, 272-275.
Hydrochloric acid: not the cause of hunger sensation, 248.
Intestine: contractions of, inhibited by excitement, 16;
innervation of, 27, 31;
use of, as test for adrenin in blood, 47-50;
contracts when empty, 251-253;
contractions of, may originate hunger sensations, 263.
Instincts: relation of, to emotions, 187, 188.
Irritability: increased in fatigued muscle by splanchnic
stimulation, 101;
neuro-muscular, lessened by fatigue, 114-117, 120;
when lowered, restored slowly by rest, 119;
when lowered, restored quickly by adrenin, 119-123, 195.
“Jumpers”: exhibition of endurance by, 223.
Mania: endurance in, 222.
Martial virtues: claims for, by militarists, 287;
importance of preserving, 290-291;
preserved in competitive sports, 297-299.
Metabolites: influence of, on muscular contraction, 104;
action of, opposed by adrenin, 129;
increase adrenal secretion, 206-208.
Militarists: emphasis of, on strength of fighting instincts,
286-288;
claims of, as to values of war, 287;
support for claims of, 287.
Muscle: weakness of, after removal of adrenal glands, 81;
improved contraction of, after injection of adrenal extract,
82;
fatigue of, 84;
method of recording fatigue of, 85-86;
fatigue of, lessened by splanchnic stimulation, 89-93;
contraction of, when fatigued, improved by increased arterial
pressure, 97-102;
irritability of, when fatigued, increased by splanchnic
stimulation, 101;
contraction of, when fatigued, lessened by decreased arterial
pressure, 102-104;
explanation of effects of varied arterial pressure on fatigued,
104-106;
irritability of, decreased in fatigue, 114-117, 120;
decreased irritability of, slowly restored by rest, 117-118,
and quickly restored by adrenin, 119-123;
contraction of fatigued denervated, increased by adrenin, 130;
point of action of adrenin in, 128-133;
use of, in struggle, 189;
energy of, from carbonaceous material, 190-193;
disappearance of glycogen from, 190;
increased efficiency of, with increase of blood sugar, 192-193;
utility of adrenin in lessening fatigue of, 194-195;
efficiency of, increased by distribution of blood in pain and
excitement, 201.
Music: stimulating influence of, 227;
influence of martial, 228.
Neurones, autonomic: extensive distribution of sympathetic, 26;
arrangement of sympathetic for diffuse action, 28;
restricted distribution of cranial and sacral, 29;
arrangement for specific action, 30.
Olympic games: as physical substitutes for warfare, 297-298.
Operations: in light anesthesia hasten coagulation of blood,
174-177.
“Ordeal of rice,” 9.
Pain: disturbing effect of, on digestion, 18-19;
as occasion for adrenal secretion, 59-62, 63;
glycosuria in, 69-70;
influence of, on distribution of blood in body, 108;
hastens coagulation of blood, 172-177;
reflex nature of responses in, 185-187;
associated with action, 189;
stimulating and depressive effects of, 189.
Pancreatic juice: flow of, inhibited by excitement, 13.
Philippine Islands: substitution of sports for warfare in, 297.
Power: the feeling of, 229.
Psychic secretion: of gastric juice, 5-8, 11;
of saliva, 6;
dependent on cranial autonomic innervation, 31.
Psychic “tone”: of gastro-intestinal muscles, 13.
Racing: relation of excitement and power in, 221.
Rage: relation of, to fear, 275;
transformation of other emotions into, 276;
bodily changes in, like those in fear, 276-277;
importance of, as a fighting emotion, 286.
Reflexes: “purposive” character of, 185-186.
“Reservoirs of power,” 216.
Respiration: utility of increased, in pain and excitement, 202;
value of forced, in lessening distress, 203.
Rest: restores irritability lessened by fatigue, 117-118.
Sacral autonomic division: functions of, in mechanisms for
emptying, 32-34;
activities of, suppressed by activities of sympathetic division,
270-272.
Saliva: psychic secretion of, 6;
importance of, for taste, 6;
flow of, inhibited by excitement, 9.
Salivary glands: innervation of, by cranial autonomic, 31.
“Second wind”: explanation of, 210.
Sex: instinct of, suppressed by fear and anger, 271.
“Sham feeding,” 5.
Splanchnic nerves: stimulation of, causes adrenal secretion,
41-43;
method of stimulating, 87-88;
stimulation of, improves contraction of fatigued muscle, 89;
stimulation of, hastens coagulation of blood, 162-167,
but not in absence of adrenal glands, 167-171;
severance of, stops rapid coagulation following excitement,
180-182;
eating after severance of, 240.
Sports: relation of excitement and power in, 219-221, 296;
as physical substitutes for warfare, 297-301;
moral values of, 300.
Stomach: psychic tonus of, 13;
contractions of, inhibited by excitement, 14-15, 17,
and by pain, 19;
innervated by sympathetic neurones, 27,
and by cranial autonomic, 31;
reference of hunger sensation to, 245-247;
emptiness of, not the cause of hunger, 248;
contractions of, when empty, 251-253;
method of recording contractions of, 255-256;
contractions of, when empty, associated with hunger sensations,
256-259;
function of contractions of empty, 263-264.
Strength: feats of, related to great emotion, 217-218, 229.
Sugar: in blood, 66, 73;
in urine, 69-76;
relation of adrenal glands to, in blood, 77;
increase of, in blood, does not hasten clotting, 159, 170;
utility of, when increased in blood, 188-193;
a source of muscular energy, 191-193;
a means of increasing muscular efficiency, 192-193;
use of, in body, not checked by adrenin, 197-199.
Swallowing: inhibits hunger sensation, 254.
Sweating: value of, in emotion and pain, 203.
“Sympathetic” autonomic division: extensive distribution of
neurones of, 26;
arranged for diffuse action, 28;
antagonistic to cranial and sacral divisions, 34-36;
active in pain and strong emotion, 36;
emotions expressed in, opposed to those expressed in cranial
and sacral divisions, 268-272;
dominance of, temporary, 273.
Threshold stimulus: as measure of irritability, 111;
method of determining, 111-114;
increased in fatigue, 114-117, 120;
when increased, slowly restored by rest, 117-118,
and quickly restored by adrenin, 119-123.
Trial by battle: feats of endurance in, 226.
Vagus nerves: severance of, does not abolish appetite, 240-241,
and does not abolish hunger contractions of the stomach, 261.
Viscera: similar changes in, in various strong emotions, 275-279;
changes in, not distinctive for emotions, 280-281.
Vomiting: in consequence of pain, 19.
Warfare: as an expression of strong emotions, 286;
physical and moral values claimed for, 287;
barbarities of, and opposition to, 289-290;
moral substitutes for, 292-293;
physical substitutes for, 293-297;
contrast between ancient and modern, 294-295.
Witnesses: stimulating influence of, 227.
Work: effect of, on neuro-muscular irritability, 117;
done with use of carbonaceous material, 190-193.
Transcriber's Notes
The following changes have been made to the text as printed.
1. Illustrations and end-of-page footnotes (marked with an asterisk)
have been located in appropriate paragraph breaks. References,
marked with numbered indices, have been re-indexed and are listed
at the end of each chapter as in the book.
2. Obvious typographical errors have been corrected.
3. Where a word is used repeatedly in the same way, spelling and
hyphenation have been made consistent, preferring the form most
often used in the printed work, or failing that the more usual form
in general use at the time of publication. No typographical change
has been made within direct quotes from other works.
4. Page 25: "or thoradico-lumbar division" has been changed to "or
thoracico-lumbar division".
5. Page 58: The name "Emden" in "Emden and v. Furth" has been
changed to "Embden" in agreement with Footnote 1 on Page 65. (Gustav
Embden, 1874-1933.)
6. Page 62: The Greek letter Β (Beta) has been substituted for
Latin B at the start of "Β-tetrahydronaphthylamine".
*** END OF THE PROJECT GUTENBERG EBOOK BODILY CHANGES IN PAIN, HUNGER, FEAR, AND RAGE ***
Updated editions will replace the previous one—the old editions will
be renamed.
Creating the works from print editions not protected by U.S. copyright
law means that no one owns a United States copyright in these works,
so the Foundation (and you!) can copy and distribute it in the United
States without permission and without paying copyright
royalties. Special rules, set forth in the General Terms of Use part
of this license, apply to copying and distributing Project
Gutenberg™ electronic works to protect the PROJECT GUTENBERG™
concept and trademark. Project Gutenberg is a registered trademark,
and may not be used if you charge for an eBook, except by following
the terms of the trademark license, including paying royalties for use
of the Project Gutenberg trademark. If you do not charge anything for
copies of this eBook, complying with the trademark license is very
easy. You may use this eBook for nearly any purpose such as creation
of derivative works, reports, performances and research. Project
Gutenberg eBooks may be modified and printed and given away—you may
do practically ANYTHING in the United States with eBooks not protected
by U.S. copyright law. Redistribution is subject to the trademark
license, especially commercial redistribution.
START: FULL LICENSE
THE FULL PROJECT GUTENBERG LICENSE
PLEASE READ THIS BEFORE YOU DISTRIBUTE OR USE THIS WORK
To protect the Project Gutenberg™ mission of promoting the free
distribution of electronic works, by using or distributing this work
(or any other work associated in any way with the phrase “Project
Gutenberg”), you agree to comply with all the terms of the Full
Project Gutenberg™ License available with this file or online at
www.gutenberg.org/license.
Section 1. General Terms of Use and Redistributing Project Gutenberg™
electronic works
1.A. By reading or using any part of this Project Gutenberg™
electronic work, you indicate that you have read, understand, agree to
and accept all the terms of this license and intellectual property
(trademark/copyright) agreement. If you do not agree to abide by all
the terms of this agreement, you must cease using and return or
destroy all copies of Project Gutenberg™ electronic works in your
possession. If you paid a fee for obtaining a copy of or access to a
Project Gutenberg™ electronic work and you do not agree to be bound
by the terms of this agreement, you may obtain a refund from the person
or entity to whom you paid the fee as set forth in paragraph 1.E.8.
1.B. “Project Gutenberg” is a registered trademark. It may only be
used on or associated in any way with an electronic work by people who
agree to be bound by the terms of this agreement. There are a few
things that you can do with most Project Gutenberg™ electronic works
even without complying with the full terms of this agreement. See
paragraph 1.C below. There are a lot of things you can do with Project
Gutenberg™ electronic works if you follow the terms of this
agreement and help preserve free future access to Project Gutenberg™
electronic works. See paragraph 1.E below.
1.C. The Project Gutenberg Literary Archive Foundation (“the
Foundation” or PGLAF), owns a compilation copyright in the collection
of Project Gutenberg™ electronic works. Nearly all the individual
works in the collection are in the public domain in the United
States. If an individual work is unprotected by copyright law in the
United States and you are located in the United States, we do not
claim a right to prevent you from copying, distributing, performing,
displaying or creating derivative works based on the work as long as
all references to Project Gutenberg are removed. Of course, we hope
that you will support the Project Gutenberg™ mission of promoting
free access to electronic works by freely sharing Project Gutenberg™
works in compliance with the terms of this agreement for keeping the
Project Gutenberg™ name associated with the work. You can easily
comply with the terms of this agreement by keeping this work in the
same format with its attached full Project Gutenberg™ License when
you share it without charge with others.
1.D. The copyright laws of the place where you are located also govern
what you can do with this work. Copyright laws in most countries are
in a constant state of change. If you are outside the United States,
check the laws of your country in addition to the terms of this
agreement before downloading, copying, displaying, performing,
distributing or creating derivative works based on this work or any
other Project Gutenberg™ work. The Foundation makes no
representations concerning the copyright status of any work in any
country other than the United States.
1.E. Unless you have removed all references to Project Gutenberg:
1.E.1. The following sentence, with active links to, or other
immediate access to, the full Project Gutenberg™ License must appear
prominently whenever any copy of a Project Gutenberg™ work (any work
on which the phrase “Project Gutenberg” appears, or with which the
phrase “Project Gutenberg” is associated) is accessed, displayed,
performed, viewed, copied or distributed:
This eBook is for the use of anyone anywhere in the United States and most
other parts of the world at no cost and with almost no restrictions
whatsoever. You may copy it, give it away or re-use it under the terms
of the Project Gutenberg License included with this eBook or online
at www.gutenberg.org. If you
are not located in the United States, you will have to check the laws
of the country where you are located before using this eBook.
1.E.2. If an individual Project Gutenberg™ electronic work is
derived from texts not protected by U.S. copyright law (does not
contain a notice indicating that it is posted with permission of the
copyright holder), the work can be copied and distributed to anyone in
the United States without paying any fees or charges. If you are
redistributing or providing access to a work with the phrase “Project
Gutenberg” associated with or appearing on the work, you must comply
either with the requirements of paragraphs 1.E.1 through 1.E.7 or
obtain permission for the use of the work and the Project Gutenberg™
trademark as set forth in paragraphs 1.E.8 or 1.E.9.
1.E.3. If an individual Project Gutenberg™ electronic work is posted
with the permission of the copyright holder, your use and distribution
must comply with both paragraphs 1.E.1 through 1.E.7 and any
additional terms imposed by the copyright holder. Additional terms
will be linked to the Project Gutenberg™ License for all works
posted with the permission of the copyright holder found at the
beginning of this work.
1.E.4. Do not unlink or detach or remove the full Project Gutenberg™
License terms from this work, or any files containing a part of this
work or any other work associated with Project Gutenberg™.
1.E.5. Do not copy, display, perform, distribute or redistribute this
electronic work, or any part of this electronic work, without
prominently displaying the sentence set forth in paragraph 1.E.1 with
active links or immediate access to the full terms of the Project
Gutenberg™ License.
1.E.6. You may convert to and distribute this work in any binary,
compressed, marked up, nonproprietary or proprietary form, including
any word processing or hypertext form. However, if you provide access
to or distribute copies of a Project Gutenberg™ work in a format
other than “Plain Vanilla ASCII” or other format used in the official
version posted on the official Project Gutenberg™ website
(www.gutenberg.org), you must, at no additional cost, fee or expense
to the user, provide a copy, a means of exporting a copy, or a means
of obtaining a copy upon request, of the work in its original “Plain
Vanilla ASCII” or other form. Any alternate format must include the
full Project Gutenberg™ License as specified in paragraph 1.E.1.
1.E.7. Do not charge a fee for access to, viewing, displaying,
performing, copying or distributing any Project Gutenberg™ works
unless you comply with paragraph 1.E.8 or 1.E.9.
1.E.8. You may charge a reasonable fee for copies of or providing
access to or distributing Project Gutenberg™ electronic works
provided that:
• You pay a royalty fee of 20% of the gross profits you derive from
the use of Project Gutenberg™ works calculated using the method
you already use to calculate your applicable taxes. The fee is owed
to the owner of the Project Gutenberg™ trademark, but he has
agreed to donate royalties under this paragraph to the Project
Gutenberg Literary Archive Foundation. Royalty payments must be paid
within 60 days following each date on which you prepare (or are
legally required to prepare) your periodic tax returns. Royalty
payments should be clearly marked as such and sent to the Project
Gutenberg Literary Archive Foundation at the address specified in
Section 4, “Information about donations to the Project Gutenberg
Literary Archive Foundation.”
• You provide a full refund of any money paid by a user who notifies
you in writing (or by e-mail) within 30 days of receipt that s/he
does not agree to the terms of the full Project Gutenberg™
License. You must require such a user to return or destroy all
copies of the works possessed in a physical medium and discontinue
all use of and all access to other copies of Project Gutenberg™
works.
• You provide, in accordance with paragraph 1.F.3, a full refund of
any money paid for a work or a replacement copy, if a defect in the
electronic work is discovered and reported to you within 90 days of
receipt of the work.
• You comply with all other terms of this agreement for free
distribution of Project Gutenberg™ works.
1.E.9. If you wish to charge a fee or distribute a Project
Gutenberg™ electronic work or group of works on different terms than
are set forth in this agreement, you must obtain permission in writing
from the Project Gutenberg Literary Archive Foundation, the manager of
the Project Gutenberg™ trademark. Contact the Foundation as set
forth in Section 3 below.
1.F.
1.F.1. Project Gutenberg volunteers and employees expend considerable
effort to identify, do copyright research on, transcribe and proofread
works not protected by U.S. copyright law in creating the Project
Gutenberg™ collection. Despite these efforts, Project Gutenberg™
electronic works, and the medium on which they may be stored, may
contain “Defects,” such as, but not limited to, incomplete, inaccurate
or corrupt data, transcription errors, a copyright or other
intellectual property infringement, a defective or damaged disk or
other medium, a computer virus, or computer codes that damage or
cannot be read by your equipment.
1.F.2. LIMITED WARRANTY, DISCLAIMER OF DAMAGES - Except for the “Right
of Replacement or Refund” described in paragraph 1.F.3, the Project
Gutenberg Literary Archive Foundation, the owner of the Project
Gutenberg™ trademark, and any other party distributing a Project
Gutenberg™ electronic work under this agreement, disclaim all
liability to you for damages, costs and expenses, including legal
fees. YOU AGREE THAT YOU HAVE NO REMEDIES FOR NEGLIGENCE, STRICT
LIABILITY, BREACH OF WARRANTY OR BREACH OF CONTRACT EXCEPT THOSE
PROVIDED IN PARAGRAPH 1.F.3. YOU AGREE THAT THE FOUNDATION, THE
TRADEMARK OWNER, AND ANY DISTRIBUTOR UNDER THIS AGREEMENT WILL NOT BE
LIABLE TO YOU FOR ACTUAL, DIRECT, INDIRECT, CONSEQUENTIAL, PUNITIVE OR
INCIDENTAL DAMAGES EVEN IF YOU GIVE NOTICE OF THE POSSIBILITY OF SUCH
DAMAGE.
1.F.3. LIMITED RIGHT OF REPLACEMENT OR REFUND - If you discover a
defect in this electronic work within 90 days of receiving it, you can
receive a refund of the money (if any) you paid for it by sending a
written explanation to the person you received the work from. If you
received the work on a physical medium, you must return the medium
with your written explanation. The person or entity that provided you
with the defective work may elect to provide a replacement copy in
lieu of a refund. If you received the work electronically, the person
or entity providing it to you may choose to give you a second
opportunity to receive the work electronically in lieu of a refund. If
the second copy is also defective, you may demand a refund in writing
without further opportunities to fix the problem.
1.F.4. Except for the limited right of replacement or refund set forth
in paragraph 1.F.3, this work is provided to you ‘AS-IS’, WITH NO
OTHER WARRANTIES OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT
LIMITED TO WARRANTIES OF MERCHANTABILITY OR FITNESS FOR ANY PURPOSE.
1.F.5. Some states do not allow disclaimers of certain implied
warranties or the exclusion or limitation of certain types of
damages. If any disclaimer or limitation set forth in this agreement
violates the law of the state applicable to this agreement, the
agreement shall be interpreted to make the maximum disclaimer or
limitation permitted by the applicable state law. The invalidity or
unenforceability of any provision of this agreement shall not void the
remaining provisions.
1.F.6. INDEMNITY - You agree to indemnify and hold the Foundation, the
trademark owner, any agent or employee of the Foundation, anyone
providing copies of Project Gutenberg™ electronic works in
accordance with this agreement, and any volunteers associated with the
production, promotion and distribution of Project Gutenberg™
electronic works, harmless from all liability, costs and expenses,
including legal fees, that arise directly or indirectly from any of
the following which you do or cause to occur: (a) distribution of this
or any Project Gutenberg™ work, (b) alteration, modification, or
additions or deletions to any Project Gutenberg™ work, and (c) any
Defect you cause.
Section 2. Information about the Mission of Project Gutenberg™
Project Gutenberg™ is synonymous with the free distribution of
electronic works in formats readable by the widest variety of
computers including obsolete, old, middle-aged and new computers. It
exists because of the efforts of hundreds of volunteers and donations
from people in all walks of life.
Volunteers and financial support to provide volunteers with the
assistance they need are critical to reaching Project Gutenberg™’s
goals and ensuring that the Project Gutenberg™ collection will
remain freely available for generations to come. In 2001, the Project
Gutenberg Literary Archive Foundation was created to provide a secure
and permanent future for Project Gutenberg™ and future
generations. To learn more about the Project Gutenberg Literary
Archive Foundation and how your efforts and donations can help, see
Sections 3 and 4 and the Foundation information page at www.gutenberg.org.
Section 3. Information about the Project Gutenberg Literary Archive Foundation
The Project Gutenberg Literary Archive Foundation is a non-profit
501(c)(3) educational corporation organized under the laws of the
state of Mississippi and granted tax exempt status by the Internal
Revenue Service. The Foundation’s EIN or federal tax identification
number is 64-6221541. Contributions to the Project Gutenberg Literary
Archive Foundation are tax deductible to the full extent permitted by
U.S. federal laws and your state’s laws.
The Foundation’s business office is located at 809 North 1500 West,
Salt Lake City, UT 84116, (801) 596-1887. Email contact links and up
to date contact information can be found at the Foundation’s website
and official page at www.gutenberg.org/contact
Section 4. Information about Donations to the Project Gutenberg
Literary Archive Foundation
Project Gutenberg™ depends upon and cannot survive without widespread
public support and donations to carry out its mission of
increasing the number of public domain and licensed works that can be
freely distributed in machine-readable form accessible by the widest
array of equipment including outdated equipment. Many small donations
($1 to $5,000) are particularly important to maintaining tax exempt
status with the IRS.
The Foundation is committed to complying with the laws regulating
charities and charitable donations in all 50 states of the United
States. Compliance requirements are not uniform and it takes a
considerable effort, much paperwork and many fees to meet and keep up
with these requirements. We do not solicit donations in locations
where we have not received written confirmation of compliance. To SEND
DONATIONS or determine the status of compliance for any particular state
visit www.gutenberg.org/donate.
While we cannot and do not solicit contributions from states where we
have not met the solicitation requirements, we know of no prohibition
against accepting unsolicited donations from donors in such states who
approach us with offers to donate.
International donations are gratefully accepted, but we cannot make
any statements concerning tax treatment of donations received from
outside the United States. U.S. laws alone swamp our small staff.
Please check the Project Gutenberg web pages for current donation
methods and addresses. Donations are accepted in a number of other
ways including checks, online payments and credit card donations. To
donate, please visit: www.gutenberg.org/donate.
Section 5. General Information About Project Gutenberg™ electronic works
Professor Michael S. Hart was the originator of the Project
Gutenberg™ concept of a library of electronic works that could be
freely shared with anyone. For forty years, he produced and
distributed Project Gutenberg™ eBooks with only a loose network of
volunteer support.
Project Gutenberg™ eBooks are often created from several printed
editions, all of which are confirmed as not protected by copyright in
the U.S. unless a copyright notice is included. Thus, we do not
necessarily keep eBooks in compliance with any particular paper
edition.
Most people start at our website which has the main PG search
facility: www.gutenberg.org.
This website includes information about Project Gutenberg™,
including how to make donations to the Project Gutenberg Literary
Archive Foundation, how to help produce our new eBooks, and how to
subscribe to our email newsletter to hear about new eBooks.
