Etches P C, Finer N N, Barrington K J, Graham A J, Chan W K
Department of Pediatrics, University of Alberta, Edmonton, Canada.
Pediatr Res. 1994 Jan;35(1):15-9. doi: 10.1203/00006450-199401000-00004.
Inhaled nitric oxide has been reported to act as a specific pulmonary vasodilator. We used the newborn piglet to create acute hypoxic pulmonary hypertension and examined the effect of inhaled nitric oxide in this model. Six newborn piglets were instrumented in order to measure cardiac index, pulmonary arterial pressure, and systemic arterial pressure. Pulmonary hypertension was induced by reducing the fraction of inspired oxygen to 0.12 to 0.14. With hypoxia (arterial oxygen saturation between 35 and 45%), pulmonary arterial pressure increased by 48% (p < 0.01), pulmonary vascular resistance increased by 74% (p < 0.01), and both systemic arterial pressure and systemic vascular resistance decreased by 38 and 31%, respectively (p < 0.01). The animals were then giving varying concentrations of inhaled nitric oxide between 5 and 80 parts per million in random order. All concentrations of nitric oxide were associated with a rapid decrease in pulmonary arterial pressure and pulmonary vascular resistance (p < 0.001). Cardiac index increased (p < 0.001) and systemic vascular resistance significantly decreased (p = 0.01) with all doses of inhaled nitric oxide. The ratio of pulmonary to systemic vascular resistance decreased with all levels of inhaled nitric oxide (p < 0.001). For all of the above observations there was no significant difference noted between the varying doses of nitric oxide. The time course of the pulmonary arterial pressure response to nitric oxide was approximately twice as fast as that seen with the inhalation of 100% oxygen (10, 50, 90% responses of 4.1, 8.8, 88.6 versus 6.7, 51.9, 197 s, respectively; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
据报道，吸入一氧化氮可作为一种特异性肺血管扩张剂。我们使用新生仔猪建立急性缺氧性肺动脉高压模型，并在此模型中研究吸入一氧化氮的作用。对六只新生仔猪进行仪器安装，以测量心指数、肺动脉压和体动脉压。通过将吸入氧分数降至0.12至0.14来诱导肺动脉高压。缺氧时（动脉血氧饱和度在35%至45%之间），肺动脉压升高48%（p<0.01），肺血管阻力升高74%（p<0.01），体动脉压和体循环血管阻力分别降低38%和31%（p<0.01）。然后，让动物随机吸入浓度在5至80 ppm之间的不同浓度一氧化氮。所有浓度的一氧化氮均与肺动脉压和肺血管阻力的快速下降相关（p<0.001）。所有剂量的吸入一氧化氮均可使心指数升高（p<0.001），体循环血管阻力显著降低（p=0.01）。随着吸入一氧化氮水平的升高，肺循环与体循环血管阻力之比降低（p<0.001）。对于上述所有观察结果，不同剂量的一氧化氮之间未发现显著差异。肺动脉压对一氧化氮反应的时间进程大约是吸入100%氧气时的两倍（10%、50%、90%反应的时间分别为4.1、8.8、88.6秒和6.7、51.9、197秒；p<0.01）。（摘要截短于250字）
