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研究慢性应激对乙醇灌胃所致胃粘膜损伤的影响并探讨其机制。方法：采用慢性束缚应激 （ｃｒｏｎｉｃ ｒｅｓｔｒａｉｎｔ ｓｔｒｅｓｓ， ＣＲＳ）法，并用７０％乙醇灌胃造成大鼠胃粘膜损伤模型。结果：①ＣＲＳ可对抗７０％乙醇灌胃 所致大鼠胃粘膜损伤，其作用具有明显的时间依赖性；双侧膈下迷走神经切除对ＣＲＳ的保护作用无影响，而腹腔 交感神经切除则使保护作用丧失。②多巴胺或异丙肾上腺素可使交感神经切除后的ＣＲＳ保护作用得到部分恢 复。去甲肾上腺素无作用；在交感神经完整大鼠，心得安或氟哌啶醇可抑制ＣＲＳ的保护作用，使用酚妥拉明无 效。③ＣＲＳ能降低正常及交感神经切除后大鼠血清胃泌素水平，但生长抑素无明显变化；ＣＲＳ对胃液总量及总酸 排出量无明显影响，但能增加胃壁结合粘液分泌。结论：ＣＲＳ时交感神经系统的激活参与了大鼠胃粘膜适应性 细胞保护，且可能通过多巴胺和肾上腺素能β受体介导，胃壁结合粘液分泌增加可能是其保护胃粘膜机制之一。
To investigate the effect of chronic stress on gastric mucosal injury induced by ethanol and its mechanism. Methods: Chronic gastric mucosa injury was induced by chronic restraint stress (CRS) and gastric perfusion with 70% ethanol. Results: ①CRS could antagonize the gastric mucosal injury induced by 70% ethanol in rats, and its effect was obviously time-dependent. Bilateral subdiaphragmatic vagotomy had no effect on the protective effect of CRS, while abdominal sympathectomy resulted in the protective effect Lost. ② dopamine or isoproterenol can sympathectomy after CRS protection was partially restored. Norepinephrine no effect; in sympathetic intact rats, propranolol or haloperidol can inhibit the protective effect of CRS, the use of phentolamine invalid. ③CRS can reduce the normal and sympathectomized rat serum gastrin levels, but no significant changes in somatostatin; CRS on the total amount of gastric juice and total acid output had no significant effect, but can increase gastric mucus secretion. CONCLUSIONS: Activation of the sympathetic nervous system during CRS is involved in the adaptive cellular protection of gastric mucosa in rats and may be mediated by dopamine and adrenergic beta receptors. Increased gastric mucosal secretion may be one of its protective mechanisms.