The potentiating actions of cigarette smoking on ethanol-induced gastric mucosal damage in rats.

Abstract

Cigarette smoking has been associated with peptic ulceration. However, the ulcerogenic mechanisms are still undefined. The aim of this study was to investigate the effects and possible mechanisms of cigarette smoke on ethanol- or cold-restraint stress-induced gastric damage. Rats were exposed to cigarette smoke followed by either an ethanol (70%) challenge or cold-restraint stress. The severity of mucosal damage, levels of prostaglandin E2 and leukotriene C4, determined by radioimmunoassay, and neutrophil infiltration in the stomach were assessed. Smoke dose-dependently potentiated ethanol-but not stress-induced ulcer. It reduced mucosal prostaglandin E2 and increased myeloperoxidase activity. Filtered cigarette smoke did not have these effects. The acidic fraction from the filters produced similar potentiating effects and also delayed ulcer healing. Mucosal leukotriene C4 and serum nicotine levels did not correlate with the mucosal injury in the stomach. Neutropenia abolished the ulcerogenic action and the increase of myeloperoxidase activity produced by both cigarette smoke and acidic fraction. Reduction of prostaglandin E2 and increase in neutrophil accumulation in the gastric mucosa are responsible for the potentiating action of acute smoke exposure on ethanol-induced gastric damage. Substances other than nicotine could contribute to these adverse reactions in the stomach.