Influence of vagotomy on mucosal protection against alcohol-induced gastric damage in the rat.

We examined the role of the vagus nerve in mediating the protective effects of subcutaneous 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) or of the mild irritant 30% ethanol (topically) against gastric mucosal injury induced by concentrated solutions of ethanol. Anesthetized rats underwent either truncal vagotomy or sham truncal vagotomy and were studied acutely or 7 days later. Under acute conditions, in rats with intact vagi, oral saline followed by 100% ethanol produced severe gastric hemorrhagic and necrotic lesions throughout the glandular gastric mucosa. Oral 30% ethanol or pretreatment with 16,16-dmPGE2 (5, 10, or 25 micrograms/kg) before giving oral saline significantly reduced the magnitude of injury when mucosa was subsequently exposed to 100% ethanol. In animals with truncal vagotomy, the protective effect of 16,16-dmPGE2 or 30% ethanol was not observed. Similar results were noted when animals were studied 7 days after sham or truncal vagotomy. In other studies, the ability of 16,16-dmPGE2 to prevent gastric injury induced by 50% ethanol or 80 mM aspirin in acid solution (160 mM HCl) with and without prior vagotomy was compared. Although 16,16-dmPGE2 (5 or 25 micrograms/kg) pretreatment significantly reduced the degree of gastric damage induced by both agents in the nonvagotomized state, and by aspirin under vagotomized conditions, only partial protection by 16,16-dmPGE2 against ethanol injury was observed in the vagotomized state. These results suggest that the mechanisms whereby prostaglandins mediate their protective effects against aspirin and ethanol may be different and that the vagus nerve influences the ability of 16,16-dmPGE2 and of the mild irritant 30% ethanol to prevent alcohol-induced gastric injury in the rat stomach.