Nitric oxide inhalation: effects on the ovine neonatal pulmonary and systemic circulations.
Nitric oxide inhalation: effects on the ovine neonatal pulmonary and systemic circulations.
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一氧化氮吸入：对绵羊新生儿肺和体循环的影响。
DOI：
10.1071/rd9960431
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Cassin,S
中科院分区：
文献类型：
--
作者：
DeMarco,V;Skimming,JW;Ellis,TM;Cassin,S
其他研究表明，吸入一氧化氮可以逆转麻醉的围产期绵羊的肺动脉高压。本研究检测了未麻醉新生羊羔正常和收缩肺循环中吸入一氧化氮的血流动力学反应。每7只羔羊进行3个试验。首先，为了确定能逆转血栓样物U46619引起的急性肺动脉高压的最小NO浓度，研究了5种不同剂量吸入NO对血流动力学的影响。其次，研究了缺氧肺血管收缩期间吸入80 ppm NO的影响。最后，为了确定吸入NO时是否会出现呼吸急促，将羔羊暴露在80 ppm NO中3小时，在此期间，通过输注U46619使肺动脉压增加一倍。在肺动脉压（PAP）正常的羔羊中，呼吸NO （80 ppm）导致肺血管阻力（PVR）轻微但显著降低。吸入浓度在10到80 ppm之间的一氧化氮6分钟（F1O2 = 0.60），当PAP与U46619一起升高时，引起PVR降低。一氧化氮选择性地作用于肺循环，即没有改变全身动脉压或任何其他测量变量。呼吸80ppm NO 6分钟可逆转缺氧肺血管收缩。在慢性暴露研究中，吸入80 ppm NO 3小时完全逆转u46619诱导的肺动脉高压。虽然在暴露于80ppm NO的3小时内，动脉血红蛋白增加，但没有迹象表明这种浓度的NO会损害氧负荷。这些数据表明，浓度低至10ppm的一氧化氮对于未麻醉的肺张力升高的新生羔羊是一种有效的、快速的、选择性的肺血管扩张剂。此外，这些数据支持使用吸入一氧化氮治疗婴儿肺动脉高压。
Others have shown that inhaled nitric oxide causes reversal of pulmonary hypertension in anaesthetized perinatal sheep. The present study examined haemodynamic responses to inhaled NO in the normal and constricted pulmonary circulation of unanaesthetized newborn lambs. Three experiments were conducted on each of 7 lambs. First, to determine a minimum concentration of NO which could reverse acute pulmonary hypertension caused by infusion of the thromboxame mimic U46619, the haemodynamic effects of 5 different doses of inhaled NO were examined. Second, the effects of inhaling 80 ppm NO during hypoxic pulmonary vasoconstriction were examined. Finally, to determine if tachyphalaxis occurs during NO inhalation, lambs were exposed to 80 ppm NO for 3 h during which time pulmonary arterial pressure was doubled by infusion of U46619. Breathing NO (80 ppm) caused a slight but significant decrease in pulmonary vascular resistance (PVR) in lambs with normal pulmonary arterial pressure (PAP). Nitric oxide, inhaled at concentrations between 10 and 80 ppm for 6 min (F1O2 = 0.60), caused decreases in PVR when PAP was elevated with U46619. Nitric oxide acted selectively on the pulmonary circulation, i.e. no changes occurred in systemic arterial pressure or any other measured variable. Breathing 80 ppm NO for 6 min reversed hypoxic pulmonary vasoconstriction. In the chronic exposure study, inhaling 80 ppm NO for 3 h completely reversed U46619-induced pulmonary hypertension. Although arterial methaemoglobin increased during the 3-h exposure to 80 ppm NO, there was no indication that this concentration of NO impairs oxygen loading. These data demonstrate that NO, at concentrations as low as 10 ppm, is a potent, rapid-action, and selective pulmonary vasodilator in unanaesthetized newborn lambs with elevated pulmonary tone. Furthermore, these data support the use of inhaled NO for treatment of infants with pulmonary hypertension.