奥美拉唑对应激状态下胃壁细胞泌酸功能的影响

 目的揭示应激状态下大鼠胃壁细胞泌酸功能的变化及奥美拉唑预防应激性溃疡的作用机制.方法将24只SD大鼠随机分为对照组、应激组和奥美拉唑组,制备水浸-束缚应激(WRS)模型,检测3组胃黏膜溃疡指数(UI)、胃液pH值和壁细胞H+,K+-ATP酶活性,观察胃黏膜组织病理变化.结果应激组UI明显升高(P＜0.01),胃液pH值明显下降(P＜0.01),壁细胞H+,K+-ATP酶活性升高(P＜0.05),镜下见胃黏膜出血坏死灶呈火山口状,几乎深达黏膜肌层.与应激组相比,奥美拉唑组UI明显下降(P＜0.01),胃液pH值明显上升(P＜0.01),壁细胞H+,K+-ATP酶活性下降(P＜0.01),镜下仅见胃黏膜充血水肿,无出血及溃疡形成.结论胃酸在应激性溃疡形成中起重要作用;奥美拉唑能有效预防应激性溃疡,其作用与抑制壁细胞H+,K+-ATP酶活性,减少胃酸分泌,从而减轻应激所致的胃黏膜损伤有关.

Effect of omeprazole on acid secretion of gastric of parietal cells in rats under stress

Objective To investigate the changes in acid secretion of gastric parietal cells and the protective effect of omeprazole against gastric stress ulcer in rats.Methods Twenty-four male SD rats were randomly divided into control group,stress group and omeprazole-treated group. Water immersion-restraint stress (WRS) model was performed, and the gastric mucosal ulcer index( UI), gastric juice pH and H + , K + -ATPase activity were determined.The structural changes in gastric mucosa were observed histopathologically. Results The UI and H+ , K+ -ATP ase activity increased significantly ( P <0.01),and pH value decreased significantly ( P <0.01) in stress group.Gastric mucosal hemorrhage and ulcer were observed , and the crateriform ulcer which almost extended to the muscular layer of mucosa was observed under light microscope in stress group.In contrast with stress group,the UI decreased and pH value increased significantly ( P <0.01),and H+ ,K+-AT-Pase activity decreased ( P < 0.05) in omeprazole-treated group. No hemorrhage or gastric ulcer but mucosal hyperaemia and edema were observed. Conclusions Gastric acid may play an important role in the formation of stress ulcer (SU). Omeprazole effectively protects gastric mucosa from injury by inhibiting H+ ,K+ -ATPase activity and reducing gastric acid secretion during stress.