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.]