THE POTENTIATING ACTIONS OF CIGARETTE-SMOKING ON ETHANOL-INDUCED GASTRIC-MUCOSAL DAMAGE IN RATS

Background & Aims: Cigarette smoking has been associated with peptic u lceration, However, the ulcerogenic mechanisms are still undefined. Th e aim of this study was to investigate the effects and possible mechan isms of cigarette smoke on ethanol- or cold-restraint stress-induced g astric damage, Methods: Rats were exposed to cigarette smoke followed by either an ethanol (70%) challenge or cold-restraint stress, The sev erity of mucosal damage, levels of prostaglandin E-2 and leukotriene C -4, determined by radioimmunoassay, and neutrophil infiltration in the stomach were assessed. Results: Smoke dose-dependently potentiated et hanol- but not stress-induced ulcer, It reduced mucosal prostaglandin E-2 and increased myeloperoxidase activity, Filtered cigarette smoke d id not have these effects, The acidic fraction from the filters produc ed similar potentiating effects and also delayed ulcer healing, Mucosa l leukotriene C-4 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 c igarette smoke and acidic fraction. Conclusions: Reduction of prostagl andin E-2 and increase in neutrophil accumulation in the gastric mucos a are responsible for the potentiating action of acute smoke exposure on ethanol-induced gastric damage. Substances other than nicotine coul d contribute to these adverse reactions in the stomach.