1907.] Further Studies of Gastrotoxic Serum. 539 



the action of the gastric juice. What that disturbance is and whether or not it 

 bears any relationship to the slight hyaline change which I have described as 

 occurring in vitro, I am not prepared to state. I think, however, that it is a 

 different process, because the action is destroyed by heat, no visible change 

 is to be seen in the cells, and an antibody is formed against it. 



If a solution of hydrochloric acid (0'5, 1, or 2 per cent.) be introduced into 

 the stomach previous to the injection of the gastrotoxic serum, the resulting 

 necrotic lesions are more pronounced than they are in the control animals 

 (fig. 4). A 2-per-cent. solution of hydrochloric acid alone produces no effect 

 whatever when introduced into the stomach of a guinea-pig. 



I think, therefore, that hyperacidity of the gastric juice must play some 

 part in the formation of gastric ulcers ; the essential factor, however, is some 

 alteration in the cell itself, and probably this alteration may be brought 

 about in a variety of ways. 



Conclusions. 



1. A gastrotoxic serum contains many precipitins which are more or less 

 specific in their actions, but these actions overlap to some extent, and absolute 

 specificity is unknown. 



2. There is no specific agglutinin for the gastric granules, the agglutination 

 being brought about by the precipitins. 



3. By repeated injection of the gastrotoxic serum, immunity is established. 

 The immune substance is present in the blood serum of the animal, its tissues 

 being still susceptible to the poison. 



It seems, therefore, impossible to establish a chronic lesion by gradual 

 absorption of the gastrotoxin, if the immunising mechanism of the animal be 

 intact. Any lesion which is produced occurs within a few hours, as I have 

 shown. If a chronic lesion occurs as the result of the action of such a cyto- 

 toxin, the explanation is probably to be found in the perpetuation of an 

 acutely produced lesion by some cause or other. Whether this cause be 

 secondary bacterial infection or hyperacidity of the gastric juice remains to 

 be proved. 



4. The actual necrosis and ulceration of the stomach is produced by the 

 gastric juice acting upon a cell which is functionally damaged. Hyperacidity 

 of the gastric juice increases the tendency to such ulceration. 



REFERENCES. 



1. Bolton, 'Roy. Soc. Proc.,' vol. 74, p. 135, 1904. 



2. Bolton, 'Roy. Soc. Proc.,' B, vol. 77, p. 426, 1906. 



3. Nuttall, " Blood Immunity and Relationship " (text-book). 



4. Deutsch, "Sur le serum antihepatique." XIII e Cong. Tnternat. de Med., Sect, de Bact. 



et Parasitol., 1900, Paris, ' Compt. Rend.,' pp. 55 — 56. 



