Bodily changes in pain, hunger, fear, and rage

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[1] 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[2] 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.

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.

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.

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).

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.

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[3] 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.[4] 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[5] 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.

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