538 Dr. C. Bolton. [June 10, 



4. The Rdle which the Gastric Juice plays in the Production of Gastric 



Ulceration. 



I have been able to prove that the actual ulceration produced by 

 injection of the gasfcrotoxic serum is brought about by the action of the gastric 

 juice. 



Although it is considered at the present day that the gastric juice plays 

 an important part in the production of gastric ulcer, I have not been able to 

 find any reliable experimental evidence in support of such a supposition. Of 

 course, it is clear that if the gastric cells are killed by any means, the gastric 

 juice will digest them, as it does any foreign proteid substance, but I refer 

 to self-digestion of the stomach, in which the gastric juice attacks a 

 gastric cell which shows no deviation from the normal on microscopic 

 examination. 



The whole question of self-digestion of the stomach is extremely interesting 

 and important, but as yet very little is known about the subject. 



Method. — My method is to neutralise the gastric juice with sodium 

 bicarbonate solution before injection of the gastrotoxic serum. 



In order to do this a soft rubber catheter is passed down the oesophagus of 

 a guinea-pig into its stomach, and about 14 c.c. of a 4-per-cent. sodium 

 bicarbonate solution introduced through a small funnel. The gastrotoxic serum 

 is then injected into the animal's peritoneal cavity. A control pig is at the 

 same time injected with the same amount of the same serum. I have done 

 eight such experiments, and in all the cases in which the gastric juice was 

 previously neutralised no necrosis of the stomach could be seen, but in all 

 the control animals the usual black patches were visible in the mucous 

 membrane of the stomach (fig. 3). 



The stomach contents in the pigs which were previously treated with 

 alkali were found to be strongly alkaline, whilst the contents of those not 

 so treated were strongly acid. I am not yet prepared to state the weakest 

 strength of the soda solution which will prevent necrosis. 



I have hitherto found no microscopic change in the stomach which precedes 

 digestion. 



These experiments conclusively prove what I had previously shown in 

 another way, namely, that the initial lesion is not a haemorrhage, for in that 

 case neutralisation of the gastric juice would certainly not prevent a 

 haemorrhage occurring. It is also well known that precipitins cause no 

 lesion on injection, because any precipitate formed would be dissolved by the 

 excess of the animal's fluids present. It appears to me that a functional 

 disturbance is set up in the gastric cells which renders them susceptible to 



