Aggravation of gastric mucosal lesions in rat stomach by tobacco cigarette smoke.

In the model of gastric mucosal injury induced by 2 mol/liter hypertonic saline in rats, we tested the hypothesis that tobacco cigarette smoke aggravates gastric mucosal lesions by inhibition of injury-induced gastric mucosal hyperemia. Experimental rats were treated with tobacco cigarette smoke or nicotine-free smoke from nontobacco cigarettes, and controls breathed room air. Gastric mucosal blood flow was measured by hydrogen gas clearance before and during the intragastric administration of hypertonic saline. Tobacco cigarette smoke 3 and 18 ml/min, but not nicotine-free smoke, significantly attenuated the hyperemia and aggravated the hypertonic saline-induced lesion in a dose-dependent manner. We then tested the hypothesis that 18 ml/min of tobacco cigarette smoke, and the dose of intravenous nicotine previously shown to block injury-induced hyperemia and aggravate 2 mol/liter saline-induced gastric damage, will also adversely affect gastric lesions induced by acidified aspirin or acidified ethanol. The results confirm that tobacco cigarette smoke and intravenous nicotine indeed aggravate gastric mucosal damage in these two models. Taken together, the data suggest that the inhibition of injury-induced hyperemia by nicotine and tobacco cigarette smoke is an important predictor of their ability to increase the susceptibility of the gastric mucosa to noxious damage. Although limited in their experimental nature, these data provide one plausible explanation for the adverse effect of tobacco cigarette smoke on peptic ulcer disease.