Prostaglandin E2 in gastric mucosa and its role in the prevention of ulcers induced by acetyl salicylic acid in cats.

Gastric mucosa of the cat generates PGE2 activity at a significantly higher concentration in the antral 59.25 +/- 7.42 ng/g) than in the oxyntic (28.06 +/- 4.50 ng/ml) gland area. Intravenous (i.v.) infusion of histamine 80 micrograms/kg/h) or intragastric (i.g.) instillation of 0.1 N HCl (4 mEq/h) for 3 h significantly decreased the generation of PGE2 in antral and fundic mucosa, but did not result in the formation of gastric lesions. Aspirin (ASA) given i.v. or i.g. for 3 h caused a further fall in the generation of PGE2 in the mucosa and when combined with i.v. histamine or i.g. HCl, it caused almost complete disappearance of PGE2 activity and the formation of antral ulcers in all tested cats. Exogenous PGE2, given i.v. in a dose (30 micrograms/kg/h) reducing histamine-stimulated (80 micrograms/kg/h) acid secretion by about 50%, prevented almost completely the formation of gastric ulcers induced by a combination of ASA plus i.v. histamine or i.g. HCl. This study indicates that the gastric mucosa generates PGE2 which is capable of preventing gastric ulcers induced by ASA combined with histamine or mucosal acidification.