左旋精氨酸甲酯及左旋精氨酸对应激状态下胃黏膜耐受性细胞保护作用的影响

目的：探讨内源性一氧化氮（NO）在应激状态下胃黏膜耐受性细胞保护中的作用及其可能的机制。方法：以重复浸水束缚应激（WRS）制作动物模型，以左旋精氨酸甲酯（L－NAME）或左旋精氨酸（L－Arg）抑制或促进内源性NO的合成，动态检测胃黏膜血流量（GMBF）、溃疡指数（UI）、黏膜一化氮含量的变化。结果：重复应激后，实验对照组大鼠UI明显下降，同时GMBF上升，黏膜内NO含量增高；L－NAME使WWRS引起的胃黏膜损伤加重，消除了GMBF的递增趋势，黏膜NO含量下降；而L－Arg可减轻WRS造成的黏膜损伤，GMBF、黏膜NO含量增相应增加；GMBF、UI、黏膜NO含量变化之间有相关关系。结论：内源性NO通过调节GMBF而介导耐受性细胞保护作用，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。

Influence of L-NAME and L-Arg on gastric mucosal tolerant cytoprotection under stress

Objective To determine the role of endogenous NO in gastric mucosal tolerant cytoprotection under stress and its possible mechanism. Methods SD rats were exposed to WRS repeatedly during which L NAME, a non selective NOs inhibitor, and L Arg, a substrate for NO synthesis, were administered to inhibit or promote the synthesis of NO, GMBF was measured using LDF 3 flowmeter, NO levels in gastric mucosa were tested by Griess reaction and gastric mucosal lesions were evaluated by ulcer index (UI). Results Gastric tolerant cytoprotection was accompanied by increased GMBF and NO levels in gastric mucosa. Inhibition of endogenous NO synthesis by L NAME worsened mucosal lesions induced by WRS. After repeated WRS, adaptive increase of GMBF was abolished and NO content in gastric mucosa significantly reduced. In contrast, enhancement of endogenous NO synthesis by L Arg attenuated mucosal erosions caused by WRS. GMBF and NO content in mucosa increased. After 4th WRS, mucosal lesions could be negligible. Conclusion By regulating GMBF, endogenous NO might play an important role in the gastric mucosal tolerant cytoprotection under stress. Inhibition of NO synthesis delayed the induction of tolerant cytoprotection, while increase NO synthesis will ptomote the induction of tolerant cytoprotection.