Abstract
Gastric emptying and gastric acid secretion in response to duodenal acidification were studied in dogs with gastric and duodenal fistulae. The duodenal fistulae were placed about 5 cm distal to the pylorus (first part of the duodenum). Three series of emptying studies were done in 5 dogs. In one series, gastric emptying of a saline meal (300 ml) was studied in response to perfusion of the second part of the duodenum and distally with amounts of 0, 4, 8, 12, and 16 mEq per hr of HC1 at a constant rate of 100 ml per hr. In the second series, only the proximal 5 cm of the duodenum was acidified, and this was accomplished by diverting an acid test meal (300 ml of 40, 80, or 120 mEq per liter of HC1) at the duodenal fistula. In the third series of tests, the acid meals were combined with acid perfusion so that the whole duodenum and proximal jejunum was acidified. Controls consisted of saline test meals (300 ml) and saline perfusion of the duodenum. Gastric emptying with acid in the first part of the duodenum was delayed, and the delay was about equal to perfusion of the rest of the duodenum. Acidification of the whole duodenum caused greatest delay in emptying, and the maximal effect was in response to 12 mEq per hr. Delay in gastric emptying with acid in the proximal 5 cm of the duodenum was rapid and sensitive, and occurred within 1 min and in response to 0.24 to 0.36 mEq of HC1. The effect of allowing acid stimulated by histamine and pentagastrin to bathe the first part of the duodenum (proximal 5 cm) was studied in 3 dogs. This was done by closing the gastric fistula and collecting from the duodenal fistula. It was found that acidification of the first part of the duodenum caused inhibition (40%) of pentagastrin- but not histamine-stimulated acid secretion. These studies indicate that the proximal 5 cm of duodenum (first part) is not only important for inhibition of acid secretion, but is also a powerful and sensitive site for inhibition of gastric emptying.
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