大鼠浸水应激性胃粘膜损伤机制的研究

本工作观察了室温下单纯束缚加生理盐水,浸水应激加生理盐水,浸水应激加阿托品(0.5mg/kg),浸水应激加酚苄明(10mg/kg),浸水应激加戊巴比妥钠(30mg/kg)5组大鼠的胃粘膜损伤程度,胃酸分泌,胃壁结合粘液分泌和胃运动的变化。结果表明:大鼠浸水应激后胃粘膜损伤严重,胃酸分泌增加,胃壁结合粘液分泌减少,胃运动亢进;预先应用阿托品再浸水应激可显著减轻胃粘膜损伤程度,抑制胃酸分泌和胃运动,但增加胃壁结合粘液的分泌;预先应用应巴比妥钠亦显著减轻胃粘膜损伤程度,抑制胃运动和增加胃壁结合粘液的分泌,但对胃酸分泌无影响;预先应用酚苄明对胃粘膜损伤程度、胃酸分泌、胃壁结合粘液分泌和胃运动均无明显影响。上述结果提示,胃运动亢进、胃壁结合粘液分泌减少及胃酸分泌增加均不同程度地参与了浸水应激性胃粘膜损伤的形成,但在胃运动受到抑制及胃壁结合粘液分泌增加的情况下,仅胃酸的存在不致引起胃粘膜严重损伤。

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.