[Studies on the mechanism of gastric mucosal injury induced by water-immersion stress in rats].

Changes in the degree of gastric mucosal injury, gastric acid output, secretion of gastric barrier mucus and gastric motility were made in 5 groups of rat: I, Restraint alone plus saline under room temperature; II, Water-immersion plus saline; III, Water-immersion plus atropine (0.5 mg/kg); IV, Water-immersion plus phenoxybenzamine (10 mg/kg); V, Water-immersion plus pentobarbital (30 mg/kg). The results were as follows: (1) Water-immersion stress resulted in severe gastric mucosal lesions, an increase in the gastric acid output, a decrease in the secretion of gastric barrier mucus and an increase in gastric motility. (2) Atropine attenuated gastric mucosal injury significantly, inhibited gastric acid output and gastric motility, while gastric barrier mucus was increased. (3) Sodium pentobarbital also significantly attenuated gastric mucosal injury and inhibited gastric motility, but had no effect on gastric acid output. (4) Phenoxybenzamine failed to affect on gastric mucosal injury, gastric acid output, gastric barrier mucus secretion and gastric motility. These results suggest that the gastric hypercontractility, the reduction of gastric barrier mucus and the increase in gastric acid output participate in varying degrees in the formation of gastric mucosal injury induced by water-immersion stress, but when gastric motility is inhibited and gastric barrier mucus increases, only the existence of gastric acid can not induce severe gastric mucosal injury.