缺氧－再给氧对大鼠胸主动脉环内皮依赖血管舒张反应的影响

生物测定法观察大鼠胸主动脉环经缺氧－再给氧、机械去内皮后，血管内皮分泌内皮细胞舒张因子（ＥＤＲＦ）的能力，ＥＤＲＦ前体Ｌ－精氨酸（Ｌ－Ａｒｇ）及拮抗剂ＮＧ－甲基－Ｌ－精氨酸（Ｌ－ＮＭＭＡ）对大鼠胸主动脉内皮ＥＤＲＦ合成和分泌的影响。发现缺氧－再给氧及去内皮的血管环对乙酰胆碱（Ａｃｈ）的舒张反应明显减弱或丧失，而对硝酸甘油的舒张反应仍保存。Ｌ－Ａｒｇ可加强正常内皮环和缺氧－再给氧环对Ａｃｈ的舒张反应；Ｌ－ＮＭＭＡ则使该作用消失。Ｌ－ＮＭＭＡ和去内皮均使血管环丧失对Ａｃｈ的舒张反应。提示缺氧－再给氧和去内皮分别可使大鼠胸主动脉内皮分泌ＥＤＲＦ机制受损或丧失，提供外源性Ｌ－Ａｒｇ有促使正常内皮和受损内皮合成和释放ＥＤＲＦ的作用。

Effect of hypoxia-reoxygenation on endothelium-dependent vasodilation in rat thoracic aortic rings

The endothelium removed by mechanical method was damaged by hypoxia-reoxygenation, in rat thoracic aortic rings.It was observed by bioassay that the ring hasthe ability of endothelial releasing endothelium-derived relaxing factor(EDRF).The effectsof L-arginine(L-Arg,precursor of EDRF)and NG-monomethyl-L-arginine(L-NMMA,competing against L-Arg)on the production and release of EDRF in the same rings wasalso surveyed.These results revealed that the vasodilation of acetylcholine(Ach)wasmarkedly reduced in hypoxic-reoxygenative rings, nearly lost in edothelial removed rings.The dose-dependent relaxation for nitroglycerin(NTG)could be seen in all aboye threetype rings.The vasodilation of Ach was obviously augmented after the normal endothelialrings and hypoxic-reoxygenative rings had be incubated with L-Arg.However,after beingincubated with L-NMMA all three type rings lost their vasodilation action of Ach.Thesestudies suggested that the mechanism of EDRF releasing was damaged by hypoxia-reoxy-genation,and lost by endothelial removal in rat thoracic aortic rings.The productionand release of EDRF was promoted by supplying exogenous L-Arg.The location ofEDRF production reside solely in vascular endothelium.