Abstract

During an investigation into the relation between the bactericidal power of serum and its antitrypsin content, Wright (1915) noted that the ability of blood to clot might be destroyed by the addition of a sufficient quantity of trypsin. Douglas and Colebrook (1916) confirmed this observation, further demonstrating that small concentrations of trypsin may have the reverse effect upon freshly draw n blood, namely, that of shortening the coagulation time. They did not analyse this phenomenon or propose an explanation for it. Both workers used a commercial pancreatic extract as the source of trypsin. Heard (1917) subsequently stated that trypsin clots oxalated plasma, but evidence has been produced (Mellanby 1935) to show that Heard’s results are explicable as being due to the presence of small quantities of calcium in the commercial preparations which he also had used. Meanwhile, Waldschmidt-Leitz, Stadtler and Steigenwaldt (1928) had concluded that fibrinogen is acted upon by trypsin in the same manner as by thrombase and had suggested the identity of, or at least close similarity between, thrombase and trypsin. Recently, Eagle and Harris (1937) have found that crystalline trypsin in suitable concentration coagulates the citrated plasma of the rabbit, guineapig, horse and man. According to them , trypsin does not coagulate fibrinogen, but activates prothrom base to thrombase in the absence of calcium.

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