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以黄嘌岭(X)-黄嘌呤氧化酶(XO)系统产生氧自由基,应用微量生物测定法观察慢性缺氧(5000m,10d)对大鼠氧自由基所致肺内动脉收缩的影响及内皮舒张因子(EDRF)在其中的作用。慢性缺氧大鼠有内皮的肺内动脉环对氧自由基的收缩反应较正常环境中的对照动物明显增强,加入EDRF灭活剂还原型血红蛋白(RHb)后更加显著;而加入超氧化物歧化酶(铜锌SOD)后则减弱,甚至消除。反之,不论加入RHb或SOD对氧自由基所致去内皮肺内动脉环的收缩反应均无明显影响。上述结果表明慢性缺氧引起肺内动脉收缩增强与EDRF有密切关系:慢性缺氧可能使EDRF的作用减弱,肺内动脉对氧自由基的反应性增强。表示EDRF及其与氧自由基的关系在慢性缺氧性肺动脉高压的形成中可能具有十分重要的意义。
Oxygen free radicals were generated from xanthine (X) -xanthine oxidase (XO) system. The effect of chronic hypoxia (5000m, 10d) on contraction of intrapulmonary arteries induced by oxygen free radicals in rats was observed by microbiological assay. Factor (EDRF) in which the role. In chronic hypoxia rats, the contractile responses to oxygen free radicals in the endosteal pulmonary artery rings were markedly enhanced compared with the control animals in the normal environment. The addition of EDRF inactivation agent reduced hemoglobin (RHb) was more pronounced; however, superoxide dismutation Enzymes (Cu, Zn SOD) then weakened, or even eliminated. On the contrary, whether adding RHb or SOD had no significant effect on the contractile response of oxygen free radicals to the arterial rings of endothelium. These results suggest that chronic hypoxia caused by enhanced pulmonary artery contractions and EDRF are closely related: chronic hypoxia may make the role of EDRF weakened, pulmonary artery oxygen free radical reactivity. That EDRF and its relationship with oxygen free radicals in the formation of chronic hypoxic pulmonary hypertension may have very important significance.