超氧阴离子抑制大鼠肠系膜阻力血管内皮依赖性舒张功能

SUPEROXIDE ANION INHIBIT ENDOTHELIUM-DEPENDENT RELAXATION IN RAT MESENTERIC ARTERY

目的:研究超氧阴离子对大鼠肠系膜阻力血管内皮细胞超极化因子(EDHF)和一氧化氮(NO)引起的血管舒张作用的影响及其可能机制。方法:雄性Sprague-Dawley大鼠,取肠系膜血管三级分支约2mm长血管环,置于DMT610M系统,记录张力变化。血管环浴液中加入焦酚建立超氧阴离子损伤模型。结果:焦酚(10,100,300和1000μmol/L)可浓度依赖性地引起乙酰胆碱(ACh)诱导的肠系膜阻力血管舒张功能减弱;其中,300μmol/L焦酚显著减弱肠系膜血管环由ACh诱导的EDHF和NO介导的内皮依赖性血管舒张效应,但对硝普钠和吡那地尔引起的内皮非依赖性的血管舒张作用无明显影响。结论:超氧阴离子可减弱阻力血管内皮依赖性舒张反应,其机制可能与超氧阴离子抑制了阻力血管内皮细胞EDHF和NO的作用有关。

Aim： To explore the resistant arterial effect of superoxide anion and its possible mechanisms. Methods： The third branch of the superior mesenteric artery in male Sprague-Dawley （200-300 g） rats was rapidly excised. Periadventitial fats and connective tissues were removed and the artery was dissected into about 2 mm rings. Each ring was dispensed between two stainless steel wires （diameter 0. 0394 mm） in a ,5 ml organ bath （DMT 610 M, Danish Myo Technology, Denmark）. Isometric force recording studies in vitro of rat mesenteric arterial rings were recorded by Powerlab Syetem. Exposure of arteries to superoxide was accomplished through the auto-oxidation of pyrogallol added to the artery baths. Then endothelium-dependent or in dependent relaxation was investigated, respectively. Results： Exposure to pyrogallol （ 10, 100, 300, and 1 000 μmol/L） which could produce superoxide anion for 15 rain resulted in a dose-dependent manner in a decrease of acetylcholine（ACh）-induced relaxation in rat mesenteric artery. Especially, the two predominant components of acetylcholine（ACh）-induced endothelium dependent relaxation, EDHF component and NO component were both inhibited by superoxide anion from pyrogallol. However, exposure to superoxide anion from pyrogallol had no effect on the endothelium-independent relaxations to pinacidil or sodium nitroprusside（SNP） in rat mesenteric artery. Conclusion： These results indicate that superoxide anion can inhibit the endothelium-dependent relaxation in rat mesenteric artery, but has no effect on the endothelium independent relaxation, in which the inhibited effect of EDHF and NO from endothelium is involved.