Cujec B, Hurst T, McCuaig R, Antecol D, Mayers I, Johnson D
College of Medicine, Department of Medicine, University of Saskatchewan, Saskatoon.
Can J Cardiol. 1997 Sep;13(9):816-24.
To assess whether inhaled nitric oxide decreases pulmonary artery pressure in patients with depressed left ventricular ejection fraction.
Randomized, blinded, crossover clinical trial.
Tertiary care university referral hospital.
Thirty-three patients with pulmonary hypertension and left ventricular dysfunction or valvular heart disease were recruited by convenience.
Systolic pulmonary artery pressure was measured by Doppler echocardiography during randomized inhalation of either 20 ppm or 40 ppm nitric oxide in 30% oxygen as well as during control periods without nitric oxide.
Systolic pulmonary artery pressure was significantly (P < 0.05) decreased with 20 ppm nitric oxide (53.4 +/- 13.9 mmHg) and 40 ppm nitric oxide (53.1 +/- 14.4 mmHg) compared with either initial control (55.8 +/- 15.3 mmHg) or terminal control (56.3 +/- 15.2 mmHg) values. The regression equation for the change in systolic pulmonary artery pressure (y) as predicted by the left ventricular ejection fraction (x) alone for 20 ppm nitric oxide was y = 13.8x-2.9; R2adj = 0.30, P < 0.0001. For 40 ppm nitric oxide alone, the regression equation was y = 16.3x-3.3; R2adj = 0.25, P < 0.0001. Left ventricular ejection fraction was the most explanatory independent variable in the multivariate equation for nitric oxide-induced change in systolic pulmonary artery pressure (R2 = 0.61, P = 0.0000). The change in systolic pulmonary artery pressure was -5.1 +/- 5.2 versus 0.8 +/- 4.9 mmHg (P < 0.0000) in patients with left ventricular ejection fractions greater than 0.25, and 0.25 or less, respectively.
These data imply that in patients with left ventricular ejection fraction of 0.25 or less, nitric oxide may not decrease systolic pulmonary artery pressure. Nitric oxide inhalation may result in a paradoxical increase in systolic pulmonary artery pressure in patients with severely depressed left ventricular ejection fraction. This effect would significantly limit the therapeutic role of nitric oxide in patients with severe heart failure.
评估吸入一氧化氮是否能降低左心室射血分数降低患者的肺动脉压。
随机、盲法、交叉临床试验。
三级医疗大学转诊医院。
通过便利抽样招募了33例患有肺动脉高压和左心室功能障碍或瓣膜性心脏病的患者。
在随机吸入20 ppm或40 ppm一氧化氮（在30%氧气中）以及无一氧化氮的对照期间，通过多普勒超声心动图测量收缩期肺动脉压。
与初始对照（55.8±15.3 mmHg）或终末对照（56.3±15.2 mmHg）值相比，20 ppm一氧化氮（53.4±13.9 mmHg）和40 ppm一氧化氮（53.1±14.4 mmHg）时收缩期肺动脉压显著降低（P<0.05）。仅由左心室射血分数（x）预测20 ppm一氧化氮时收缩期肺动脉压变化（y）的回归方程为y = 13.8x - 2.9；校正R² = 0.30，P<0.0001。仅对于40 ppm一氧化氮，回归方程为y = 16.3x - 3.3；校正R² = 0.25，P<0.0001。在一氧化氮诱导的收缩期肺动脉压变化的多变量方程中，左心室射血分数是最具解释力的独立变量（R² = 0.61，P = 0.0000）。左心室射血分数大于0.25和0.25或更低的患者，收缩期肺动脉压变化分别为-5.1±5.2与0.8±4.9 mmHg（P<0.0000）。
这些数据表明，对于左心室射血分数为0.25或更低的患者，一氧化氮可能不会降低收缩期肺动脉压。吸入一氧化氮可能会导致左心室射血分数严重降低的患者收缩期肺动脉压出现反常升高。这种效应将显著限制一氧化氮在严重心力衰竭患者中的治疗作用。
