Abstract
Conclusions
From the results described in this paper, it appears evident that peptone produces shock in the dog by a mechanism very similar to that leading to anaphylactic shock. Participation of the white blood elements (leucocytes and platelets) in the discharge of histamine and heparin from liver cells is definitely suggested by the fact that the severity of the shock is closely connected with the incapacity of those blood elements to return to blood stream, and also by experiments with isolated liver, in which it became apparent that peptone is unable by itself to release those substances from liver cells, and that the presence and retention of blood elements (leucocytes and platelets) is an indispensable step leading to the discharge of those substances. That the final mediator for the release of these substances is activated plasma trypsin is strongly suggested by the fact that platelets contain a kinase for plasma trypsin and that there actually occurs activation of this enzyme, as shown by fibrinolysis occurring after the injection of peptone. Also the fact that fibrinolysis is maximal after the first injection of peptone, moderate after a second injection and minimal or absent after a third injection, constitutes strong evidence that activation of plasma trypsin is actually concerned in the mechanism of production of the shock and that desensitization which occurs in those kinds of shock is probably dependent upon exhaustion of the capacity for activation of plasma trypsin. Experiments upon those lines are being actively conducted in this laboratory.
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