一氧化氮对急、慢性缺氧大鼠血流动力学及缺氧性肺血管收缩反应的影响

EFFECTS OF INHALEDNITRIC OXIDE ON HEMODYNAMICS AND HYPOXICPULMONARY VASOCONSTRICTION IN ACUTEAND CHRONIC HYPOXIC RATS

观察了吸入０．００４％的一氧化氮（ＮＯ）对急、慢性缺氧大鼠血流动力学、缺氧性肺血管收缩反应（ＨＰＶ）、血气及高铁血红蛋白（ＭｅｔＨｂ）的影响。结果表明：（１）常氧吸入ＮＯ时能明显降低慢性缺氧大鼠肺动脉平均压（Ｐｐａ）和肺血管阻力（ＰＶＲ），但对正常大鼠的Ｐｐａ和ＰＶＲ无明显影响；（２）慢性缺氧大鼠急性缺氧时ＨＰＶ较正常大鼠弱，吸入ＮＯ不但降低两者的急性缺氧肺动脉高压，且完全逆转两者的ＨＰＶ；（３）吸入ＮＯ对急、慢性缺氧大鼠体循环血流动力学、血气及ＭｅｔＨｂ含量无明显影响。提示吸入ＮＯ能选择性降低急、慢性缺氧性肺动脉高压，且逆转ＨＰＶ。

The effects of inhalation of 0.004% nitric oxide(NO)on hemodynamics,hypoxic pulmonaryvasoconstriction(HPV)blood gas and plasma methemoglobin(MetHb)level in acute as well aschronic hypoxic rats were investigated.The results were as follows:1.The mean pulmonary arte-rial pressure(P pa)and pulmonary vascular resistance(PVR)were signiflcantly decreased by in-haled NO in chronic hypoxic rats(P<0.01),but these changes were not observed in normoxiccontrol rats.2.The HPV was weaker in chronic hypoxic rats than that in control animals.Thepulmonary arterial hypertension induced by acute hypoxia was lowered greatly and HPVstrengthened by acute hypoxia was reversed completely by inhalation of NO in both chronichypoxic and control rats.3.There was no effect on systemic arterial pressure,systemic vascularresistance,PaO_2,PaCO_2 and MetHb level in acute and chronic hypoxic rats inhaling NO.It issuggested that the pulmonary arterial hypertension induced by acute and chronic hypoxia couldbe lowered selectively and the HPV induced by hypoxia could be reversed by inhalation of 0.004%NO in rats.