THE VAGUS NERVE AND ITS NONCHOLINERGIC MECHANISM IN THE MODULATION OFETHANOL-INDUCED GASTRIC-MUCOSAL DAMAGE IN RATS

The role of the cholinergic pathway in the vagus nerve in modulating g astric lesion formation by ethanol was examined, using an ex-vivo stom ach chamber preparation. Subdiaphragmatic vagotomy significantly incre ased the lesion areas but lowered acid secretion and gastric mucosal b lood flow (GMBF). Atropine had no effect, whereas pirenzepine antagoni zed ethanol-induced mucosal damage. All three procedures showed simila r potencies in depressing acid secretion, but only pirenzepine reverse d the fall in the GMBF produced by ethanol. These differential effects of vagotomy, atropine and pirenzepine on gastric function suggest tha t the cholinergic component in the vagus nerve may not be important in the formation of ethanol-induced gastric damage. The persistent prote ctive action as well as the restoration of ethanol-induced GMBF drop b y pirenzepine in vagotomized animals further support this hypothesis. The worsening effect of vagotomy is probably modulated by a non-cholin ergic mechanism, the abolition of which makes the gastric mucosa more susceptible to damage by ethanol. The acid-independent protective acti on of pirenzepine and its influence on the GMBF, which were not exhibi ted by atropine, are indeed unique and perhaps may be attributed to th is non-cholinergic pathway.