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本工作在离体灌流肺动脉环模型及培养的牛肺动脉内皮细胞探讨内皮舒张因子 (EDRF/NO)在缺氧肺动脉收缩中的作用。结果发现 ,在内皮完整血管环加入NO合成抑制剂L NNA(10 -4mol/L)、NO合成前体L Arg(10 -2 mol/L)分别升高 (+ 80 % ,P <0 .0 1)和降低 (-35 % ,P <0 .0 5 )缺氧肺动脉收缩幅度 ;给予硝酸甘油 (10 -4 mol/L)直接补充NO可降低缺氧肺动脉收缩幅度 ,此效应可被可溶性鸟苷酸环化酶抑制剂亚甲蓝部分逆转 ;用Northern印渍杂交技术显示缺氧使培养的牛肺动脉内皮细胞NO合成酶(NOS)基因表达明显受抑。结果提示缺氧时NOS基因表达受抑及NO合成释放降低可能是缺氧肺动脉收缩的发生机制之一。
This study was to investigate the role of endothelium relaxing factor (EDRF / NO) in hypoxic pulmonary artery contraction in isolated perfused pulmonary artery rings model and cultured bovine pulmonary artery endothelial cells. The results showed that NO synthesis inhibitor L NNA (10 -4 mol / L) and NO synthesis precursor L Arg (10 -2 mol / L) were increased (+80%, P <0. 1) and decreased (-35%, P <0.05) hypoxic pulmonary arteries contractility. Nitric acid glycerol (10 -4 mol / L) supplemented NO directly reduced the hypoxic pulmonary artery contractile amplitude, which could be induced by soluble Cytoplasmic reversion of the nucleotidase was partially reversed. Northern blotting showed that the expression of NO synthase (NOS) gene in cultured bovine pulmonary artery endothelial cells was significantly inhibited by hypoxia. The results suggest that hypoxia, NOS gene expression inhibition and decreased NO synthesis and release may be one of the mechanisms of hypoxic pulmonary artery contraction.