SHOCK 37 



be induced by the action of mustard in the stomach, 

 and, as the author has shown (Turck, 1902) that in 

 such experiments the exudate which first forms is not 

 a good medium for the growth of bacteria, it seems 

 more reasonable to postulate that in gastritis the ap- 

 parent general toxemia is due to endocellular sub- 

 stances released from the cells injured by the meta- 

 bolic activities of the microorganisms. 



Such a concept is in agreement with the well known 

 fact that bacterial toxins, with the exception of that 

 formed by B. botulinus, are not absorbed through 

 the gastrointestinal tract. 



Early in the history of anesthesia, it was recognized 

 that a state of profound shock may be induced by the 

 anesthetic. In 1866, Sabaarth reported 119 cases of 

 death during chloroform anesthesia, less than half 

 of which appeared to be due to a direct toxic effect 

 of the anesthetic. In the same year Nothnagel reported 

 that inhalation, or injection of chloroform and ether, 

 produced a fatty degeneration of various organs. So 

 far as we know, the experiments of the latter author 

 were the first to demonstrate the specific toxic action 

 of these anesthetics upon the body cells. 



Early in the author's career, he was impressed by 

 the fact that some experimental animals showed evi- 

 dence of shock more readily than others of the same 

 species, even comparatively trivial manipulation 

 under anesthesia resulting in shock and subsequent 

 death a day or two later. As it seemed likely that such 

 results were due largely to the effect of the anesthetic 

 per se, the latter were investigated in the absence of ex- 

 perimental surgery. (Turck, 1903b.) 



A series of healthy dogs were kept under deep 



