PHYSIOLOGY AND BIOCHEMISTRY OF SHOCK 439 



should take into account the chain of events which occur in anaphylac- 

 tic shock following the antigen-antibody reaction within or about the 

 cells. The steps preceding anaphylactic shock must occur with tre- 

 mendous speed. In anaphylaxis, the antigen-antibody reaction is 

 claimed to occur in contact with the cells. The critical question re- 

 volves around the problem of how the combination of an antigen 

 with an antibody fixed on tissue cells ushers in a chain of explosive 

 reactions fatal to the host. Particularly critical is the question of how 

 a perfectly harmless native tissue cathepsin is turned into a destructive 

 agent by the antigen-antibody reaction. The proponents of the theory 

 of proteolytic histamine liberation assume that cathepsin exists in an 

 inactive state until an antigen-antibody combination takes place. In 

 consequence of the immune reaction the activation of cathepsin is 

 supposed to take place. The observation of Jobling and Petersen 

 (1914) is cited to the effect that specific precipitates can activate plasma 

 trypsin by adsorption or inactivation of plasma antitrypsin which, ac- 

 cording to Jobling and Petersen, is a lipid, and not the serum trypsin 

 inhibitor, a polypeptide of 6000 molecular weight. It is possible that 

 "plasma trypsin" of Jobling and Petersen is activated by the antigen- 

 antibody complex by removing the antitryptic lipid. This is not surpris- 

 ing in view of the findings of Horsfall and Goodner (1935, 1936) that 

 lipids are part of the precipitate formed by the combination of type 

 specific pneumococcal polysaccharide and horse and rabbit antipneu- 

 mococcal serum. The removal of lipids from the antipneumococcal 

 horse serum caused a loss of a power of agglutination and precipitation, 

 and a marked reduction in these activities with rabbit serum. The 

 activities of the former system could be restored by the addition of 

 lecithin; the latter system was likewise activated by the addition of 

 cephalin. Hilleman and Nigg (1948) reported that antigens extracted 

 vdth ether from the suspensions of yolk-sacs infected with the virus 

 of lym-'pho granuloma venereum, completely inactive in complement 

 fixation test, were activated by the addition of: (a) alcohol soluble 

 lipoid from the same extract; (b) alcohol soluble lipoid from normal 

 yolk-sacs; and, (c) lecithin obtained from soybeans. The maximal 

 reactivity of the purified antigenic fraction depended on the presence 

 of lecithin in optimal concentration. The importance of lecithin for the 

 activity of other complement-fixing systems has been reported. Pang- 

 born (1942) found that purified cardio-lipin, entirely inactive in itself 



