血管内皮舒张因子在氧自由基所致慢性缺氧大鼠肺内动脉收缩中的作用

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。

ROLE OF ENDOTHELIUM-DERIVED RELAXING FACTOR IN THE CONTRACTIONS OF INTRAPULMONARY ARTERY INDUCED BY OXYGEN-DERIVED FREE RADICALS IN CHRONIC HYPOXIC RAT

The role of endothelium-derived relaxing factor (EDRF) on the effect of oxy-gen-derived free radicals (generated by xanthine-xanthine oxidase system) on intrap-ulmonary arterials in chronic hypoxic rats was studied by a microbioassay method.Intrapulmonary artery rings with intact or denuded endothelium of hypoxic (5 000m, 10 days) and normoxic rats were prepared for observation of oxygen-derived freeradicals induced contraction. It was shown that oxygen-derived free radicalsinduced contractions of intrapulmonary arterial rings with intact endotheliumwere obviously augmented in hypoxic rats than in normoxic controls. Theaugmented responses could be further potentiated by the addition of EDRFinactivator reduced hemoglobin (RHb), but diminished or even abolished byapplying superoxide dismutase (Cu-Zn SOD). However, no effect on denudedrings was observed when RHb or SOD was added. It is concluded thatchronic hypoxia may attenuate the action of EDRF in the enhancement of thereactivity of intrapulmonary artery to oxygen-derived free radicals.