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Inhaled nitric oxide reduces pulmonary artery pressures in portopulmonary hypertension.

机译:吸入一氧化氮可降低肺动脉高压中的肺动脉压力。

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摘要

Pulmonary artery hypertension in association with liver failure (portopulmonary hypertension [PPHTN]) is a significant barrier to liver transplantation because patients with this condition have a very high mortality when transplantation is undertaken. Inhaled nitric oxide (NO), a potent pulmonary vasodilator, reduces pulmonary artery pressure (PAP) in some patients with primary pulmonary hypertension, but its effect in patients with PPHTN is controversial. We investigated the hemodynamic effects of inhaled NO in 6 patients with PPHTN. Five of 6 patients responded to NO inhalation with decreases in PAP and pulmonary vascular resistance of greater than 10%; these decreases were statistically significant at NO concentrations of 10 and 30 ppm. Cardiac output did not significantly change. We conclude that inhalation of NO reduces PAPs in some patients with PPHTN.
机译:伴有肝功能衰竭的肺动脉高压(肺动脉高压[PPHTN])是肝移植的重要障碍,因为患有这种疾病的患者在进行移植时死亡率很高。吸入性一氧化氮(NO)是一种有效的肺血管扩张剂,可降低某些原发性肺动脉高压患者的肺动脉压力(PAP),但其对PPHTN患者的作用尚存争议。我们调查了6例PPHTN患者吸入NO的血液动力学效应。 6例患者中有5例对NO吸入有反应,PAP降低且肺血管阻力大于10%;在NO浓度为10和30 ppm时,这些下降具有统计学意义。心输出量没有明显变化。我们得出的结论是,吸入NO可以降低某些PPHTN患者的PAP。

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