应激状态下NO的胃粘膜保护作用及其与壁细胞泌酸的关系

目的:探讨应激状态下一氧化氮(NO)的胃粘膜保护作用及其与壁细胞泌酸的关系.方法:采用水浸-束缚应激(WRS)方法制备应激性溃疡(SU)动物模型,检测胃粘膜溃疡指数(UI)、胃粘膜NO含量和壁细胞H ,K -ATPase活性,观察L-硝基精氨酸甲酯(L-NAME)和L-精氨酸(L-Arg)对应激后大鼠壁细胞H ,K -ATPase活性及胃粘膜损伤的影响.结果:L-NAME(20 mg·kg-1)可使胃粘膜NO含量减少(P＜0.01),壁细胞H ,K -AT-Pase活性增加(P＜0.05),并加重应激所致的胃粘膜损伤;L-Arg(300 mg·kg-1)则使胃粘膜NO含量增加(P＜0.01),壁细胞H ,K -ATPase活性下降(P＜0.05),减轻应激所致胃粘膜损伤.结论:NO对应激状态下大鼠胃粘膜具有保护作用,其机制与抑制壁细胞H ,K -ATPase活性有关.

Protective effect of nitric oxide on gastric mucosa and its relationship to the acid secretion of gastric parietal cells under stress in rats

Aim: To demonstrate the protective effect of nitric oxide(NO) on gastric mucosa and its relationship to the acid secretion of parietal cells under stress in rats. Methods: Water immersion-restraint stress(WRS) model in SD rats was performed. The gastric mucosal ulcer index(UI), NO contents in gastric mucosa and H~ , K~ -ATPase activity of parietal cells were measured. The effects of N~G-nitro-L-arginine methyl ester(L-NAME) and L-arginine(L-Arg) on the H~ , K~ -ATPase activity of parietal cells and stress-induced gastric mucosal lesion were observed. Results: L-NAME pretreatment decreased NO contents in gastric mucosa, activated H~ , K~ -ATPase activity of parietal cells and aggravated gastric mucosal lesion, whereas L-Arg pretreatment increased NO contents, inhibited H~ , K~ -ATPase activity and significantly ameliorated stress-induced gastric mucosal lesion. Conclusion:WTBZ] Endogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H~ , K~ -ATPase activity of parietal cells. JP]