REFERENCES
[1] Gruber: American Journal of Physiology, 1913, xxxii, p. 437.
[2] E. L. Porter: American Journal of Physiology, 1912, xxxi, p. 149.
[3] Cannon and Nice: American Journal of Physiology, 1913, xxxii, p. 55.
[4] Albanese: Archives Italiennes de Biologie, 1892, xvii, p. 239.
[5] Abelous and Langlois: Archives de Physiologie, 1892, xxiv, pp. 269–278, 465–476.
[6] Radwánska: Anzeiger der Akademie, Krakau, 1910, pp. 728–736. Reviewed in the Centralblatt für Biochemie und Biophysik, 1911, xi, p. 467.
[7] Panella: Archives Italiennes de Biologie, 1907, xlvii, p. 30.
[8] Langley: Proceedings of the Royal Society of London, 1906, lxxviii, B, p. 181. Journal of Physiology, 1905–6, xxxiii, pp. 374–413.
[9] 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[1] 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[2] 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[3] for adrenin given by mouth was subjected to a single test on man by Dale and Laidlaw,[4] 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[5] 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.