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目的：观察无水乙醇引起胃粘膜损伤的病理改变，并探讨其引起胃粘膜损伤的可能机理。方法：以正常大鼠为对照，观察无水乙醇引起的大鼠急性胃粘膜损伤的病理及扫描电镜改变，并测定胃粘膜中的前列腺素E2（PGE2）、生长抑素（SS）、胃粘膜表面粘液及胃粘膜血流（GMBF）。结果：无水乙醇可直接引起胃粘膜表面上皮细胞的变性、坏死及脱落；无水乙醇组与对照组比较胃粘膜中的PGE2（P<0．05）、SS（P＜0．05）、胃粘膜表面粘液（P<0．05）、GMBF（P＜0．05）均明显降低。结论：无水乙醇可直接损伤大鼠胃粘膜表面的上皮细胞。其引起大鼠急性胃粘膜损伤的机理可能与无水乙醇引起胃粘膜内PGE2、SS、胃表面粘液及GMBF降低，从而损伤胃粘膜的防御功能有关。
Objective: To observe the pathological changes of gastric mucosal injury induced by ethanol and to explore the possible mechanism of gastric mucosal injury. Methods: The normal rats were used as the control to observe the pathological changes of acute gastric mucosal injury induced by ethanol and the change of the scanning electron microscope (SEM). The levels of prostaglandin E2 (PGE2), somatostatin (SS), gastric mucosa Surface mucus and gastric mucosal blood flow (GMBF). Results: Absolute ethanol could directly cause degeneration, necrosis and shedding of epithelial cells on the gastric mucosa. Compared with the control group, absolute ethanol could reduce PGE2 (P <0.05), SS (P <0.05) Gastric mucosal mucus (P <0.05), GMBF (P <0.05) were significantly lower. Conclusion: Absolute ethanol can directly damage the epithelial cells on the gastric mucosal surface of rats. The mechanism of acute gastric mucosal injury in rats may be related to the decrease of PGE2, SS, gastric mucus and GMBF in gastric mucosa caused by absolute ethanol, which may impair the defense function of gastric mucosa.