The mechanism of vagotomy-induced acute gastric mucosal injury in the rat.

The present study investigated the integrity of the rat gastric mucosa after 6 hours of vagotomy without drainage. Transection vagotomy was employed to ensure complete gastric vagal denervation. Vagotomy without drainage produced gastric distension and mucosal injury confined to the glandular part. Anterior truncal vagotomy produced injury in 70% of rats, whereas truncal or transection vagotomy produced injury in all rats. The injury score with transection vagotomy was significantly higher than that with anterior truncal (21.2 mm2 +/- 1.6 vs. 8 mm2 +/- 2.7, mean +/- SEM, n = 10, p less than .01) or truncal vagotomy (21.2 mm2 +/- 1.6 vs. 15.6 mm2 +/- 1.4, mean +/- SEM, n = 10, p less than .05). Histologic examination of the mucosal injury revealed necrosis involving the epithelium and lamina propria. Cholestyramine, pyloroplasty, or gastric diversion protected the stomach against the vagotomy-induced mucosal injury. The results demonstrate in the rat that vagotomy without drainage produces within 6 hours injury of the gastric mucosa, which increases as vagal denervation is rendered more complete. Because cholestyramine protects the rat stomach against vagotomy-induced acute gastric mucosal injury, reflux of duodenal contents appears to be the principal factor behind this injury. Pyloroplasty prevents gastric distension but probably not duodenal contents refluxing, suggesting that this distention also may have a role in the mechanism of the said injury.