Hare Joshua M, Nguyen Geoffrey C, Massaro Anthony F, Drazen Jeffrey M, Stevenson Lynne W, Colucci Wilson S, Fang James C, Johnson Wendy, Givertz Michael M, Lucas Caroline
Johns Hopkins Medical Institutions, Baltimore, Maryland 21287, USA.
J Am Coll Cardiol. 2002 Sep 18;40(6):1114-9. doi: 10.1016/s0735-1097(02)02117-4.
We sought to test the hypothesis that patients with decompensated heart failure (HF) lose a compensatory process whereby nitric oxide (NO) maintains pulmonary vascular tone.
Exhaled nitric oxide (eNO) partially reflects vascular endothelial NO release. Levels of eNO are elevated in patients with compensated HF and correlate inversely with pulmonary artery pressures (PAP), reflecting pulmonary vasodilatory activity.
We measured the mean mixed expired NO content of a vital-capacity breath using chemiluminescence in patients with compensated HF (n = 30), decompensated HF (n = 7) and in normal control subjects (n = 90). Pulmonary artery pressures were also measured in patients with HF. The eNO and PAP were determined sequentially during therapy with intravenous vasodilators in patients with decompensated HF (n = 7) and in an additional group of patients with HF (n = 13) before and during administration of milrinone.
The eNO was higher in patients with HF than in control subjects (9.9 +/- 1.1 ppb vs. 6.2 +/- 0.4 ppb, p = 0.002) and inversely correlated with PAP (r = -0.81, p < 0.00001). In marked contrast, patients with decompensated HF exhibited even higher levels of eNO (20.4 +/- 6.2 ppb) and PAP, but there was a loss of the inverse relationship between these two variables. During therapy (7.3 +/- 6 days) with sodium nitroprusside and diuresis, hemodynamics improved, eNO concentrations fell (11.2 +/- 1.2 ppb vs. before treatment, p < 0.05), and the relationship between eNO and PAP was restored. After milrinone, eNO rose proportionally with decreased PAP (p < 0.05).
Elevated eNO may reflect a compensatory circulatory mechanism in HF that is lost in patients with clinically decompensated HF. The eNO may be an easily obtainable and quantifiable measure of the response to therapy in advanced HF.
我们试图验证这样一个假设，即失代偿性心力衰竭（HF）患者失去了一种由一氧化氮（NO）维持肺血管张力的代偿机制。
呼出一氧化氮（eNO）部分反映血管内皮释放的NO。代偿性HF患者的eNO水平升高，且与肺动脉压（PAP）呈负相关，反映肺血管舒张活性。
我们使用化学发光法测量了代偿性HF患者（n = 30）、失代偿性HF患者（n = 7）和正常对照者（n = 90）肺活量呼吸时的平均混合呼出NO含量。还测量了HF患者的肺动脉压。在失代偿性HF患者（n = 7）以及另一组HF患者（n = 13）中，于静脉应用血管扩张剂治疗期间以及米力农给药前和给药期间，依次测定eNO和PAP。
HF患者的eNO高于对照组（9.9±1.1 ppb对6.2±0.4 ppb，p = 0.002），且与PAP呈负相关（r = -0.81，p < 0.00001）。与之形成显著对比的是，失代偿性HF患者的eNO水平（20.4±6.2 ppb）和PAP更高，但这两个变量之间失去了负相关关系。在硝普钠和利尿剂治疗期间（7.3±6天），血流动力学得到改善，eNO浓度下降（11.2±1.2 ppb对治疗前，p < 0.05），eNO与PAP之间的关系得以恢复。使用米力农后，eNO随PAP降低而成比例升高（p < 0.05）。
eNO升高可能反映了HF中的一种代偿性循环机制，而在临床失代偿性HF患者中这种机制丧失。eNO可能是晚期HF中对治疗反应的一种易于获取且可量化的指标。
