无水乙醇引起大鼠急性胃粘膜损伤的机理研究

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。

Study of mechamism of acute gastric mucosa lesion caused by anhydrous alcohol in rats

Objective:To observe the pathological changes of gastric mucosa caused by anhydrous alcohol and to study the possible mechanism of acute gastric mucosa lesion. Methods:Compared with the normal ones,pathological and scanning electrol microscope changes of gastric mucosa in rats with acute gastric mucosa lesion caused by anhydrous alcohol were observed, and the Prostaglandin E2 (PGE2),Somatotatin(SS), gastric mucosa blood flow (GMBF) and the mucus on the gastric mucosa surface were determined. Results: Anhydrous alcohold could directly cause degeneration,necrosis and exfoliation of epithelia in the gastric mucosa surface. PGE2 (P<0. 05),SS(P<0. 05),the mucus on the gastric mucosa surface (P<0. 05) and GMBF (P<0. 05) in the tested rats were much less than those in normal ones. Conclusion: Anhydrous alcohol can directly deteriorate the epithelia in the gastric mucosa surface of rats. The possible mechanism may be related to the decrease of PGE2,SS,GMBF and mucus of gastric mucosa surface dut to anhydrous alcohol,which deteriorate the gastric mucosa barrier further.