THE EFFECT OF INHALED NITRIC-OXIDE ON THE PULMONARY CIRCULATION OF THE NEONATAL PIG

THE EFFECT OF INHALED NITRIC-OXIDE ON THE PULMONARY CIRCULATION OF THE NEONATAL PIG
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DOI:
10.1203/00006450-199401000-00006
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发表时间:
1994-01-01
期刊:
影响因子:
3.6
通讯作者:
DAWSON, CA
DAWSON, CA
中科院分区:
医学3区
文献类型:
--
作者:
NELIN, LD;MOSHIN, J;DAWSON, CA

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为了研究在新生儿肺动脉高压模型中吸入低水平一氧化氮(NO)的肺血管扩张剂选择性,我们将麻醉的自主呼吸新生猪依次暴露于四种不同吸入的ps混合物中的每一种:室内空气,含百万分之二十五的NO的室内空气,缺氧(14%O2的N2),和缺氧与25百万分之一的NO。室内空气,室内空气与NO,缺氧,缺氧与NO暴露的持续时间为15分钟。进行了以下测量:平均体循环动脉、平均肺动脉和楔压;热稀释心输出量;食管压力;气管流量;动脉PO 2、PCO 2 pH、血红蛋白和高铁血红蛋白。在室内空气和缺氧条件下,吸入NO均降低肺动脉压(平均肺动脉压16 +/- 1 mmHg室内空气,13 +/- 1 mmHg室内空气+NO,p < 0.005;平均肺动脉压21 +/- 2 mmHg缺氧,14 +/- 1 mmHg缺氧+NO,p < 0.005)。在控制或缺氧条件下,NO对体循环动脉压、心输出量、动态肺顺应性、肺阻力或测量的血液变量均无显著影响。结果表明,吸入NO是一种选择性肺血管扩张剂,能有效地逆转急性缺氧性肺血管收缩反应。通过吸入NO产生的含氧量正常的血管舒张也表明在麻醉的自主呼吸的新生猪中存在基础血管紧张素。使用的短期暴露没有产生可检测到的毒副作用表现。
To study the pulmonary vasodilator selectivity of low levels of inhaled nitric oxide (NO) in a model of neonatal pulmonary hypertension, we sequentially exposed anesthetized, spontaneously breathing neonatal pigs to each of four different inspired ps mixtures: room air, room air with 25 parts per million NO, hypoxia (14% O2 in N2), and hypoxia with 25 parts per million NO. The room air, room air with NO, hypoxia, and hypoxia with NO exposures were of 15-min duration. The following measurements were made: mean systemic arterial mean pulmonary arterial, and wedge pressures; thermodilution cardiac output; esophageal pressure; tracheal flow; and arterial PO2, PCO2 pH, hemoglobin, and methemoglobin. Inhalation of NO decreased pulmonary arterial pressure in both room air and hypoxia conditions (mean pulmonary arterial pressure 16 +/- 1 torr room air, 13 +/- 1 torr room air with NO, p < 0.005; and mean pulmonary arterial pressure 21 +/- 2 torr hypoxia, 14 +/- 1 torr hypoxia with NO, p < 0.005). NO had no significant effect on systemic arterial pressure, cardiac output, dynamic lung compliance, pulmonary resistance, or the measured blood variables during either control or hypoxic conditions. The results indicate that inhaled NO was a selective pulmonary vasodilator that could effectively reverse acute hypoxic pulmonary vasoconstriction. The normoxic vasodilation produced by NO inhalation also indicates the existence of basal vasomotor tone in the anesthetized, spontaneously breathing neonatal pig. The short-term exposures used produced no detectable manifestations of toxic side effects.