Lipopolysaccharide-induced gastroprotection is independent of the vagus nerve

This study was done to examine the role of the vagus nerve in a model of ga stric injury during endotoxemia. In conscious rats, lipopolysaccharide (LPS ; 20 mg/kg ip) treatment for 5 hr prevented macroscopic gastric injury caus ed by acidified ethanol (150 mM HCl/50% ethanol). In addition, LPS enhanced gastric luminal fluid accumulation, decreased gastric mucosal blood flow ( laser Doppler), and increased plasma gastrin levels (radioimmunoassay). Sub diaphragmatic truncal vagotomy, performed 7 days prior to LPS inhibited LPS -induced fluid accumulation, further reduced gastric mucosal blood flow fol lowing LPS, and augmented LPS-induced gastrin release compared to those in pyloroplasty controls. Atropine (1 mg/kg ip) prevented LPS-induced fluid ac cumulation but did not influence the effects of LPS on blood flow or gastri n release. Neither vagotomy nor atropine negated LPS-induced gastroprotecti on. This is the first report to examine the role of cholinergic nerves in t he stomach during endotoxemia. The data indicate that LPS causes accumulati on of gastric luminal fluid in part through its effects on cholinergic nerv es, In contrast, the effects of vagotomy on blood flow and gastrin release following LPS involve a noncholinergic pathway. However, LPS-induced gastro protection is independent of the vagus nerve.