Abstract
In previous communications one of us 1 , 2 called attention to the importance of gastric inhibition due to stimuli acting in the duodenum, in the regulation of gastric emptying. In the case of acid and certain other chemical stimuli the inhibition was found to be due to an “enterogastric” reflex over the vagus nerves. Later the present authors with Dr. Mogan 3 reported additional experimental evidence leading to the same conclusions and added proof that the normal duodenal contents following a meal of raw lean beef act as adequate stimuli to cause gastric inhibition. Experiments were reported which indicate that the inhibitory effect is in part due to chemical stimuli, the nature of which was not determined. The present study is an effort to identify the inhibitory agent.
The type of animal preparation and the methods used are described in the previous reports.
Brunemeier and Carlson 4 observed that 10% Witte's peptone in 0.2% HCl, when injected into the duodenum, stopped gastric hunger contractions. In experiments performed in July, 1935, we attempted to use Witte's peptone as a buffering agent for HCl solutions to be used in a further study of gastric inhibition from the duodenum. We found that the peptone, even in neutral solution, caused inhibition of gastric peristalsis.
In those experiments, after a meal of raw lean beef, the duodenum (of dogs) was perfused through its lumen with various solutions, using normal saline as a control. Fig. 1 (Exp. of July 24, 1935,) shows the effect on antral peristalsis of changing the perfusion fluid from normal saline to 0.5% Witte's peptone in neutral solution.
A further study of this phenomenon has been made by injecting 10 cc. quantities of distilled water solutions of various commercial peptones into the first part of the duodenum of dogs with the stomach empty or shortly after feeding a meal of dog biscuit. Witte's peptone, “Proteose” peptone, “Bacto” peptone and a granular peptone produced by a French manufacturer have been investigated.
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