Blood coagulation time and its acceleration by adrenin and pain

He argued that skin is exposed to damage often enough that a specific set of nerves for skin pain needs no special explanation. In his view such nerves present no genetic difficulty, any more than the clotting of blood or innate immunity.¹ Clotting here counts as an accepted product of selective adaptation to injury. Sherrington gives no measurement of it, and he does not link it to nerves or glands.

Cannon (1915) tested whether adrenin has any effect on the rate of coagulation. Earlier experiments in the book had shown that pain and emotional excitement raise the secretion of adrenin into the blood.⁴ In the injection experiments, rapid clotting appeared directly after minute doses.² Larger doses behaved differently. They could first produce slower clotting, followed in turn by a much shorter coagulation time.³ Cannon also reported that stimulating the splanchnic nerves, with the accompanying rise in adrenal secretion, gave more rapid clotting of blood.⁴

Bayliss (1915) approached clotting through ions. He cited the effect of calcium ions on clotting as a case where even a closely related element such as barium cannot replace calcium.⁵ In another passage he listed coagulation time among the properties that neutral salts alter in emulsoids, together with surface tension and viscosity. He linked these changes to the distribution of water between the two phases of the system.⁶ Loeb (1916) used the term differently. He judged it quite probable that very high temperature coefficients near the upper limit of life express the coagulation time of certain proteins.⁷

Hill (1926), in Muscular Activity, used clotting as an analogy. He asked the reader to imagine that a shock produces, possibly through the lactic acid that results from it, a coagulation of some element of the muscle fibre, analogous to the clotting of blood plasma.⁸ Hill used clotting as a familiar analogy for a sudden change in a colloid.