The role of the vagus nerve in the protective action of acid inhibitors on ethanol‐induced gastric mucosal damage in rats

Abstract

The role of vagus in the actions of different acid inhibitors on ethanol-induced gastric damage and mucosal blood flow (GMBF) changes was studied in anaesthetized rats, using an ex vivo stomach chamber preparation. Subdiaphragmatic bilateral vagotomy decreased the basal gastric acid secretion and GMBF; it also intensified ethanol-evoked lesions in the glandular mucosa. Misoprostol, omeprazole and cimetidine produced a similar degree of reduction in acid output. Misoprostol given subcutaneously (s.c.) (50 micrograms/kg), or added to the incubation solution (12.5 micrograms) for 15 min, markedly prevented ethanol-induced lesion formation and reduction in GMBF. The reversing effect of s.c. injection of misoprostol on either lesion formation or on GMBF reduction was attenuated by vagotomy. Omeprazole protected against lesion formation only when present in the incubation solution (12.5 mg) of ex vivo chamber preparations of both vagus-intact and vagotomized animals, but the effect was significantly less in the latter group. The drug also prevented the depressive action of ethanol in vagus-intact animals. Cimetidine pretreatment (50 mg s.c. or 12.5 mg in incubation solution), however, did not modify the effects of ethanol on lesion formation and the GMBF. The findings indicate that the three different types of acid inhibitors exert different actions on ethanol-induced gastric mucosal damage, although they produced similar inhibition of acid output. Vagotomy lowers the GMBF and attenuates the antiulcer action of misoprostol and omeprazole, especially when the drugs are given by the parenteral route.

Study of the Gastrointestinal Protective Effects of Polysaccharides from Angelica sinensis in Rats

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H2-Blocker modulates heart rate variability

“…The secretion of gastric acid has been known to be closely related to autonomic nervous tone, especially to vagal tone [9,10]. If such a relation is strong enough, the change in gastric juice pH may well induce change in autonomic nervous tone.…”

Central and peripheral vagal mechanisms involved in gastric protection against ethanol injury

“…Evidence for central vagal gastric protective mechanisms was also demonstrated by acute ablation of the dorsal motor nucleus of the vagus (DMN) or vagotomy, which potentiated gastric lesion formation induced by EtOH 6 , 7 . In addition, an intact vagus is essential for the gastroprotective effect of prostaglandins (PG) 8 –10 . The growing literature on the central action of specific peptides to regulate gastric function through vagal pathways 11 served as a major focal point to advance our understanding of central and peripheral mechanisms underlying vagal‐dependent gastric protections 12 –14 .…”