PHYSIOLOGY AND BIOCHEMISTRY OF SHOCK 415 



According to Dubois-Ferriere (1945), trauma to the hind Hmbs of 

 rabbits under conditions of venous occlusion leads to a fall of 

 blood pressure. The blood shows an increase in adenosine triphos- 

 phate, acetylcholine, and potassium ion derived from the damaged 

 tissue. 



The most significant change in blood chemistry during shock is an 

 increase in plasma amino nitrogen, which is related to the failure of the 

 liver to assimilate amino acids for protein and oxidative metabolism. 

 During the development of shock catabolic changes in the tissues with 

 respect to inorganic phosphate, pentose, glucose, amino acid nitrogen 

 and lactic and pyruvic acid have been found (McShan, et ah, 1945). 

 During the anoxia of hemorrhagic hypotension in dogs there is a de- 

 struction of liver enzymes and coenzymes, in particular, destruction 

 of cocarboxylase (dephosphorylation), cozymase, alloxazine adenine 

 dinucleotide and an inactivation of the protein moities of amino acid 

 oxidase and lactic dehydrogenase (Greig and Govier, 1943; De Turk 

 and Greig, 1945; Alexander, 1944). Le Page (1946a, 1946b) reported 

 that the tissues of animals in shock exhibit greatly elevated inorganic 

 phosphate and lactic acid, depleted glycogen, adenosine triphosphate 

 and phosphocreatine, and possess an abnormal accumulation of phos- 

 phopyruvic acid. Of the tissues examined brain, heart, muscle, kidney 

 and liver, in the terminal stages of Noble-Collip, tourniquet, and 

 hemorrhagic shock, the liver showed the most complete depletion of 

 the stores of adenosine triphosphate compounds and other sources of 

 readily available energy. In the biochemical sense, complete exhaustion 

 of energy reservoirs— adenosine polyphosphates— means the death of 

 tissue (Le Page, 1946b). McShan, et al. (1945) and Meyer, et at. 

 (1946) hypothesize that the essential feature of fatal shock is the 

 critical exhaustion of the supplies of readily available energy, in the 

 form of phosphocreatine and adenosine triphosphate. 



7. Acetylclioline in Anaphylactic Shock 



Various investigators have reported that anaphylactic shock is ac- 

 companied by the liberation of acetylcholine (Went and Lissak, 1936; 

 Farber et ah, 1944). Danielopolu (1947a) claims to have demon- 

 strated that the liberation of acetylcholine is the direct cause of 

 anaphylactic shock and that histamine plays a secondary role. It may 



