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应用生物测定法观察黄嘌呤(X)-黄嘌呤氧化酶(XO)系统产生的氧自由基对正常、缺氧(5000m,10d)Wistar大鼠肺内动脉环张力的影响及内皮细胞在其中的作用。发现XO在一定浓度范围内产生的氧自由基可引起肺内动脉剂量依赖性收缩。正常鼠肺内动脉去内皮或加内皮舒张因子 (EDRF) 灭活剂后,此剂量依赖性收缩明显增强。慢性缺氧大鼠肺内动脉无论内皮完整与否,上述收缩反应均增强。提示缺氧使内皮细胞和(或)EDRF的功能受到损害。应用超氧化物歧化酶(铜锌SOD),在正常或缺氧鼠肺内动脉上可分别加强或恢复内皮细胞抑制氧自由基的缩血管作用。提示慢性缺氧时,内皮细胞和(或)EDRF受到超氧阴离子的严重破坏,这一机制可能在缺氧性肺动脉高压的形成中起重要作用。
The effects of oxygen free radicals produced by xanthine (X) -xanthine oxidase (XO) system on the pulmonary arterial ring tension in normal and hypoxic (5000m, 10d) Wistar rats were observed by bioassay and the effects of endothelial cells effect. Oxygen radicals produced by XO at a range of concentrations were found to cause a dose-dependent contraction of the pulmonary arteries. The dose-dependent contractions of the normal rat intrapulmonary artery were significantly decreased with or without EDRF inactivation. Chronic hypoxia in the pulmonary arteries regardless of endothelial integrity or not, the contraction response were enhanced. Hypoxia impaired the function of endothelial cells and / or EDRF. Application of superoxide dismutase (CuZn SOD), in the normal or hypoxic rat pulmonary arteries can respectively strengthen or restore endothelial cells inhibit the vasoconstriction of oxygen free radicals. It is suggested that the endothelial cells and / or EDRF are severely damaged by superoxide anion in chronic hypoxia, and this mechanism may play an important role in the formation of hypoxic pulmonary hypertension.