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.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
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)
作者简介
陆国明（1966-），男，浙江嘉兴人，副教授，医学硕士，主要从事应激性溃疡病理生理研究。
