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为探讨胃粘膜血流量 (GMBF)在应激状态下胃粘膜耐受性细胞保护中的作用及其可能的调节因子 ,采用重复浸水束缚应激 (WRS)制作动物模型 ,以左旋硝基精氨酸甲酯 (L NAME)或左旋精氨酸 (L Arg)抑制或促进内源性NO的合成 ,动态检测GMBF、溃疡指数 (UI)、粘膜NO含量的变化。结果显示 :①重复应激后 ,实验对照组大鼠UI明显下降 ,同时GMBF上升 ,粘膜NO含量增高。②L NAME使WRS引起的胃粘膜损伤加重 ,GMBF的适应性增加反应消失 ,粘膜NO含量明显下降。③L Arg可减轻WRS造成的粘膜损伤 ,GMBF、粘膜NO含量均相应增加。④GMBF、UI、粘膜NO含量变化之间有相关关系。提示GMBF在应激状态下胃粘膜耐受性细胞保护中有重要作用 ,内源性NO是其调节因子之一 ;L NAME抑制其合成 ,延缓这一作用 ,L Arg增加其合成 ,促进该作用
To investigate the role of gastric mucosal blood flow (GMBF) in the protection of gastric mucosal-tolerant cells under stress and its possible regulators, the animal model was established by repeated immersion restraint stress (WRS) L NAME or L Arg inhibited or promoted the synthesis of endogenous NO, and dynamically detected the changes of GMBF, ulcer index (UI) and mucosal NO content. The results showed: (1) After repeated stress, the experimental control group rats UI decreased significantly, while GMBF increased mucosal NO content increased. ② L NAME increased WRS-induced gastric mucosal injury, GMBF increased response to the disappearance of response, mucosal NO decreased significantly. ③ L Arg can reduce the WRS mucosal injury, GMBF, mucosal NO content increased accordingly. ④ GMBF, UI, mucosal NO content changes have a correlation between. It is suggested that GMBF plays an important role in the protection of gastric mucosal-tolerant cells under stress. Endogenous NO is one of its regulators. L-NAME inhibits its synthesis and delays this effect. L Arg increases its synthesis and promotes this effect