PHYSIOLOGY AND BIOCHEMISTRY OF SHOCK 423 



and does not prevent the action of acetylcholine and histamine on 

 the blood pressure and circulation, but does so in conjunction with 

 atropine. On this basis, the suggestion is made that therapeutically in 

 anaphylactic shock both should be given, since, after atropinization, 

 acetylcholine and histamine cause adrenalin secretion from the 

 adrenals (Danielopolu, Popesco, and Mezinesco, 1941-1945). 



According to Danielopolu (1947a, 1947b, 1947c), liberation of 

 acetylcholine is the primary factor of anaphylaxis, and the production 

 of histamine is a secondary factor; there is no histamine production 

 w^ithout acetylcholinogenesis. The phenomenon of anaphylactic shock 

 is identical with that provoked by an excitation of the parasympathetic 

 system (which reacts by a liberation of acetylcholine): inhibition of 

 the heart hy auriculo-ventricular (A-V) hlock, hypotension, hyper- 

 mohility of digestive and vesical systems and uterus, and leucopenia 

 involving mononucleosis and eosinophilia. Intravenous injection of 

 acetylcholine produces the above named symptoms resembling (with- 

 out being identical) those produced by anaphylactic shock. Intra- 

 trachial injection of acetylcholine into guinea pigs produces a respir- 

 atory syndrome similar to anaphylaxis: expiratory dyspnea, hronchial 

 rales, asphyxia, etc. Autopsy reveals pulmonary lesions identical with 

 those which he found in anaphylactic shock. 



A simple mechanical excitation of the tissue provokes the phe- 

 nomenon of acetylcholinogenesis. Intravenous injection of antigens 

 and injection of a suspension of gelatin liberate acetylcholine. Eserine 

 and strophanthin favor anaphylaxis by inhibiting cholinesterase, 

 whereby a greater concentration of acetylcholine in the tissues ac- 

 cumulates. Atropine in higher doses blocks anaphylaxis by block- 

 ing the cells of the terminal organs. Adrenalin in small doses favors 

 anaphylaxis and blocks it in large doses. A hyperconcentration of 

 acetylcholine and, secondarily, of adrenalin precursor accompany 

 anaphylaxis. 



In this connection it must be pointed out that Loewi and Navratil 

 (1926) showed decisively that inhibition of the heart resulting from 

 vagal stimulation is due to the liberation of acetylcholine. It was 

 also demonstrated that the heart muscle contained choline-esterase 

 which rapidly hydrolyzed acetylcholine after its liberation, limiting 

 the duration of its action. The action of this esterase was inhibited by 

 prostigmine (eserine). 



