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,
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[Footnote 124: Zuntz: Oppenheimer’s Handbuch der Biochemie, Jena,
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[Footnote 125: Benedict and Cathcart: Muscular Work, a Metabolic
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[Footnote 126: Chauveau and Kaufmann: Comptes Rendus, Académie des
Sciences, 1886, ciii, p. 1062.]
[Footnote 127: Comptes Rendus, Société de Biologie, 1886, xxxviii,
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[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
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[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.]