【摘要】 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。更多还原

【Abstract】 s Objective: To study the effect of chronic stress on the ethanol induced gastric mucosa damage and analysis the peripheric mechanism. Methods: Chronic restraint stress (CRS) was carried out and the mode of gastric mucosa damage was made by intragastric 70% ethanol in at. Results: ①The gastric mucosa damage by ethanol was significant attenuated af- ter the rats had receivsed CRS for 4 or 7 days. The protection of CRS was not affected in rats with Vagotomy but disappareds in sympathectomized rats. ② Adminitration of isoprenaline or dopamine before CRS could partially, and norepinephrine could not, restore the protection sin sympathectomized rats. In rats with intact sympathetic nerve, preinjection of haoperidel or propranolol inhibited CBS induced protection which, however, was not affected by phentalamine. ③The level of plasma gastrin was decreased in both nomal and sympathectomized rats after CRS. But the plasma somatostain was not changed. CRS also promote thse secretion of gastric mucus. But there is no effect on the secretion of gastric juice and gastric acid. Conclusion : The aetivation of sympathetic nervous system mediated the adaptive cytoprotection of gastric mucosa in CRS tats and the effect are probably mediated through β and doparminhe receptors. The increase of gastric mucus secretion is also possibly one of the mechanism osf protect gastric mucosa of CRS.更多还原