摘要
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 。
To determine the role of GMBF in gastric mucosal tolerant cytoprotection under stress and its possible regulator, SD rats were exposed to repeated WRS, during which L NAME , a non selective NOS inhibitor, or L Arg, a substrate for NO synthesis, was administered to inhibit or promote the synthesis of NO, GMBF was measured using LDF 3 Flowmeter, NO level in gastric mucosa was monitored by Griess reaction, and gastric mucosal lesions were evaluated by UI. The results showed that gastric tolerant cytoprotection was accompanied by increased GMBF and NO level 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 produced by WRS and GMBF, NO content in mucosa increased. Good relationships between the changes in GMBF, UI, NO content in mucosa were found. It suggested that GMBF might play an important role in gastric mucosal tolerant cytoprotection. Endogenous NO might be one of its regulators. Inhibition of its synthesis delayed the induction of tolerant cytoprotection, while enhancementpromoted it.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2001年第6期410-412,共3页
Medical Journal of Chinese People's Liberation Army
基金
军队医药卫生杰出中青年人才基金资助课题 !(编号 1996卫科训字 95 )
