Effect of synthetic 15-methyl analog of prostaglandin E2 on gastric secretion and peptic ulcer formation.

Abstract In conscious cats with chronic gastric and pancreatic fistulas, a synthetic 15-methyl analog of prostaglandin E 2 , 15/S/15-methyl-E 2 -methyl ester, caused a dose-related inhibition of maximal gastric acid and pepsin response to pentagastrin and histamine. The administration of 1.0 μg per kilogram-hour of 15-Me-PGE 2 produced complete inhibition of acid secretion induced by pentagastrin and about 80 per cent inhibition of secretion induced by histamine. Gastric secretion in response to peptone meal (measured by intragastric titration) reached a level similar to that induced by histamine. 15-Me-PGE 2 caused profound decrease of acid response to a meal. The inhibitory action of the analog occurred after either intravenous or intraduodenal administration. The compound prevented the formation of duodenal peptic ulcer induced by 36-hour intravenous infusion of pentagastrin or histamine, but did not affect pancreatic response to exogenous secretin or duodenal acidification. The antisecretory and anti-ulcer action of the compound is likely to be a direct one on the parietal cell and it could prove of value in the treatment of peptic ulcer.