Inhaled nitric oxide reverses pulmonary vasoconstriction in the hypoxic and acidotic newborn lamb.
Inhaled nitric oxide reverses pulmonary vasoconstriction in the hypoxic and acidotic newborn lamb.
复制标题
吸入一氧化氮可以逆转缺氧和酸中毒的新生羔羊的肺血管收缩。
DOI：
10.1161/01.res.72.2.246
复制
发表时间：
1993
影响因子：
20.1
通讯作者：
Zapol,WM
中科院分区：
文献类型：
--
作者：
RobertsJr,JD;Chen,TY;Kawai,N;Wain,J;Dupuy,P;Shimouchi,A;Bloch,K;Polaner,D;Zapol,WM
我们确定吸入低水平的一氧化氮（NO）气体是否可以选择性地逆转近期新生羔羊的缺氧肺血管收缩，以及呼吸性酸中毒是否会减弱血管舒张。为了研究空气和一氧化氮诱导出生后不久肺血管舒张的机制，我们测量了新生通气胎羊的血浆和肺cGMP水平。在FIO2 0.10呼吸时，新生羔羊的肺血管阻力指数几乎翻了一番，肺血流主要是通过减少动脉导管的左向右血流来减少的。在FIO2 0.10下吸入20 ppm NO，几分钟内完全逆转缺氧肺血管收缩。最大的肺血管舒张发生在吸入>或= 80ppm NO时。在FIO2 0.10时呼吸8%的二氧化碳，将肺血管阻力指数提高到与FIO2 0.10时呼吸相同的水平，而不添加二氧化碳。呼吸性酸中毒对吸入NO后肺血管舒张无减弱作用。在我们的研究中，吸入一氧化氮没有引起全身性低血压或升高高铁血红蛋白水平。在胎羊肺内开始空气通气4分钟后，cGMP浓度几乎翻了一番，而血浆cGMP浓度没有改变。在FIO2 0.21下，80ppm NO通气使肺和血浆cGMP浓度增加了三倍。我们的数据表明，吸入NO气体是一种快速而有效的选择性血管舒张剂，新生儿肺循环由于缺氧和呼吸性酸中毒而升高血管张力，通过增加肺部cGMP浓度起作用。
We determined whether inhaling low levels of nitric oxide (NO) gas could selectively reverse hypoxic pulmonary vasoconstriction in the near-term newborn lamb and whether vasodilation would be attenuated by respiratory acidosis. To examine the mechanism of air and NO-induced pulmonary vasodilation soon after birth, we measured plasma and lung cGMP levels in the newly ventilated fetal lamb. Breathing at FIO2 0.10 nearly doubled the pulmonary vascular resistance index in newborn lambs and decreased pulmonary blood flow primarily by reducing left-to-right blood flow through the ductus arteriosus. Inhaling 20 ppm NO at FIO2 0.10 completely reversed hypoxic pulmonary vasoconstriction within minutes. Maximum pulmonary vasodilation occurred during inhalation of > or = 80 ppm NO. Breathing 8% CO2 at FIO2 0.10 elevated the pulmonary vascular resistance index to a level similar to breathing at FIO2 0.10 without added CO2. Respiratory acidosis did not attenuate pulmonary vasodilation by inhaled NO. In none of our studies did inhaling NO produce systemic hypotension or elevate methemoglobin levels. Four minutes after initiating ventilation with air in the fetal lamb lung, cGMP concentration nearly doubled without changing preductal plasma cGMP concentration. Ventilation with 80 ppm NO at FIO2 0.21 increased both lung and preductal plasma cGMP concentration threefold. Our data suggest that inhaled NO gas is a rapid and potent selective vasodilator of the newborn pulmonary circulation with an elevated vascular tone due to hypoxia and respiratory acidosis that acts by increasing lung cGMP concentration.