PHYSIOLOGY AND BIOCHEMISTRY OF SHOCK 403 



the dog, loss of coagulability and multiple small subserous hemorrhages 

 are features common to both types of shocks (Biedl and Kraus, 1909; 

 Feldberg and O'Connor, 1937; Dragstedt and Mead, 1937). In 

 the intact dog, administration of peptone causes a release of hista- 

 mine into the blood, a decrease in liver histamine and a marked 

 thrombocytopenia (Holmes, Ojers and Dragstedt, 1941). Gotzl and 

 Dragstedt (1942) reported the liberation of histamine from rabbit 

 white cells in vitro on addition of peptone, and in vivo, peptone caused 

 a fall in whole blood histamine and thrombocytopenia. Jacques and 

 Waters (1941) observed that heparin is produced in peptone shock. 

 In peptone and anaphylactic shock, the occurrence of a short period 

 of hypercoagulability, agglutination and the ensuing disappearance 

 from the blood of the platelets which contain most of the histamine, 

 suggested to Quick (1942) the concept that, in either type of shock, 

 the sudden liberation of histamine causes the agglutination of platelets. 

 The agglutinated masses of platelets are carried to the capillary beds of 

 the liver, lung and spleen and other tissues where disintegration begins 

 and thromboplastin and histamine are liberated. The former substance 

 is responsible for the short period of observed hypercoagulability, and 

 the latter for certain of the various symptoms observed in these shocks. 

 In peptone shock there is a marked decrease in the volume of oxygen 

 consumed by the animals, and a simultaneous increase in the lactic acid 

 content of blood. The relation of these changes to the mechanism of 

 shock will be discussed below. 



3. Shocks Caused by Proteolytic Enzymes 



a. Trypsin. The pharmacological action of proteolytic enzymes, 

 particularly of trypsin, has been variously studied. The findings of 

 Dragstedt and Wells (1944) can be summarized in the following para- 

 graphs. In unanesthetized dogs, the intravenous injection of trvpsin 

 results in vomiting, urination, defecation and collapse, comparable to 

 that occurring in anaphylaxis. In anesthetized dogs, the injection of 

 trypsin results in prompt and profound fall in systemic blood pressure, 

 with little or no change in pulmonary artery pressure, congestion of 

 the liver and a corresponding congestion of the viscera. Injection of a 

 given amount of trypsin into a branch of the portal vein in the dog 

 was followed by a much more conspicuous and lasting fall of carotid 



