Topical 16,16-dimethyl PGE2 prevents alcohol-induced damage in canine gastric mucosa

Abstract

Using a canine Heidenhain pouch model, we examined the effect of pretreatment with topical administration of 16,16-dimethyl prostaglandin E2 (dmPGE2) on gastric mucosal damage induced by 15% ethanol in acid solution. Ethanol alone damaged the pouches, as was evidenced by large net fluxes of Na+ and K+ into the pouch, loss of H+ from the bathing solution, and an increase in gastric perfusate volume. Topical dmPGE2 by itself had no effect on H+ or K+ flux, but significantly increased the flux of Na+ and stimulated volume output. These effects on Na+ and volume were not increased further during exposure of the mucosa to ethanol, and the changes in K+ flux and H+ loss induced by ethanol alone were completely prevented by dmPGE2. We conclude that topically applied dmPGE2 prevents alcohol-induced damage to the canine gastric mucosa. The mechanism underlying this protection remains unknown, but the observation that dmPGE2 stimulated a volume flow rich in Na+ suggests that this secretion in some way prevented the permeation of H+ ions with their damaging effects on gastric mucosal cells.