Yang G, Chen G, Wang D
Department of Emergency, Tongji Hospital, Tongji Medical University, Wuhan 430030.
J Tongji Med Univ. 2000;20(3):197-9. doi: 10.1007/BF02886987.
To investigate the effects of prostaglandins (PGs) and leukotrienes (LTs) on hypoxic pulmonary vasoconstriction (HPV), in vivo rats experiment and in vitro perfused lung experiment were conducted. The effect of hypoxia on hemodynamics, concentrations of TXB2 and 6-keto-PGF1 alpha in serum and lung tissue during hypoxia and effects of PGs and LTs on HPV were observed. The results showed that pulmonary arterial pressure (Ppa) and pulmonary vascular resistance were increased during hypoxia, but cardiac output and systemic arterial pressure were decreased. There were increases of the concentrations of TXB2 and 6-keto-PGF1 alpha and their ratio in serum and lung tissue during hypoxia. After use of cyclooxygenase inhibitor (indomethacin) in vivo and in vitro, HPV was augmented respectively, but after use of lipoxygenase inhibitor (diethylcorbamazine) or leukotriene receptor blocker (LY-171883), HPV was attenuated. It was suggested that LTs mediated pulmonary vasoconstriction, PGs inhibited pulmonary vasoconstriction and they played a modulating role during hypoxia.
为研究前列腺素（PGs）和白三烯（LTs）对缺氧性肺血管收缩（HPV）的影响，进行了体内大鼠实验和体外灌注肺实验。观察了缺氧对血流动力学的影响、缺氧期间血清和肺组织中TXB2和6-酮-PGF1α的浓度以及PGs和LTs对HPV的影响。结果表明，缺氧期间肺动脉压（Ppa）和肺血管阻力增加，但心输出量和体动脉压降低。缺氧期间血清和肺组织中TXB2和6-酮-PGF1α的浓度及其比值升高。体内和体外使用环氧化酶抑制剂（吲哚美辛）后，HPV分别增强，但使用脂氧化酶抑制剂（二乙氨苯嗪）或白三烯受体阻滞剂（LY-171883）后，HPV减弱。提示LTs介导肺血管收缩，PGs抑制肺血管收缩，它们在缺氧过程中起调节作用。
