Role of prostaglandins in the formation of aspirin-induced gastric ulcers

Abstract

Gastric mucosa of the rat generates both PGE2 and PGI2 activity in significantly higher concentrations in the antrum than in the fundus. Aspirin, given intravenously or intragastrically in doses producing gastric mucosal lesions, causes a dose-dependent decrease in the generation of mucosal PGE2 and PGI2, which is further enhanced by gastric perfusion of HCl. Exogenous PGE2 and PGI2 administered intravenously in doses not affecting gastric secretion almost completely prevented the formation of aspirin-induced ulcers. This study indicates that gastric mucosa is capable of generating PGE2 and PGI2 which may be responsible for its protection against chemical injury.