ADVERSE-EFFECTS OF VAGOTOMY ON ETHANOL-INDUCED GASTRIC INJURY IN THE RAT - ABSENCE OF A ROLE FOR GLUTATHIONE REDOX CYCLE

Truncal vagotomy is known to aggravate the damaging effects of alcohol -induced gastric injury and prevent the occurrence of adaptive cytopro tection against such injury by a mild irritant This study was undertak en to determine whether aberrations in glutathione (GSH) metabolism we re responsible for these vagotomy-induced effects. Fasted rats (6-8/gr oup) were subjected to truncal vagotomy and pyloroplasty or sham vagot omy and pyloroplasty. One week later they were given 2 ml of oral sali ne or the mild irritant 25% ethanol (EtOH). Thirty minutes following s uch treatment, animals were either sacrificed or orally received 2 ml of 100% EtOH and then were sacrificed 5 min later. At sacrifice, in ea ch experimental group, stomachs were removed and either evaluated macr oscopically for the degree of injury involving the glandular gastric e pithelium or samples of the mucosa were prepared for measurement of to tal GSH levels or GSH peroxidase (GPX) and GSH reductase (GRT) activit y. In nonvagotomized animals, saline treatment prior to 100% EtOH expo sure resulted in injury to the glandular epithelium involving approxim ately 18%. Treatment with 25% EtOH prior to 100% EtOH exposure virtual ly abolished this injury. In vagotomized animals, 100% EtOH elicited a lmost three times the amount of injury observed in the nonvagotomized state and the protective effect of 25% EtOH pretreatment was prevented . Effects of the various treatment modalities on GPX and GRT activity were not significantly different from control values. When mucosal GSH results were plotted against the presence or absence of gastric injur y among the various groups studied, no significant correlation was app arent. Thus, aberrations in glutathione metabolism do not explain the absence of adaptive cytoprotection following vagotomy or the exacerbat ion of alcohol-induced damage under conditions of vagal denervation.