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  

PROTECTIVE EFFECT OF NITRIC OXIDE ON GASTRIC MUCOSA AND ITS RELATIONSHIP TO THE ACID SECRETION OF GASTRIC PARIETAL CELLS UNDER STRESS IN RATS

作　　者：陆国明[1] 李玉梅[2] 郭连军[1] 章明[3] 

机构地区：[1]嘉兴学院医学院,浙江嘉兴314001 [2]武警浙江省总队医院消化内科,浙江嘉兴314000 [3]浙江大学医学院解剖学教研室,浙江杭州310031

出　　处：《中国应用生理学杂志》2005年第3期301-304,共4页Chinese Journal of Applied Physiology

基　　金：浙江省科技厅资助项目(G20030081);浙江省嘉兴市科技计划资助项目(20031061)

摘　　要：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(20mg.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(300mg.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。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 mueosa 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 sigrtificandy ameliorated stress-induced gastric mucosal lesion,Conclusion：Endogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H^＋,K^＋-ATPase activity of parietal cells.

关 键 词：应激 应激性溃疡 一氧化氮 壁细胞 H^+ K^+-ATPase 

分 类 号：R363.2[医药卫生—病理学]