Pulmonary hemodynamic responses to brain natriuretic peptide and sildenafil in patients with pulmonary arterial hypertension
Pulmonary hemodynamic responses to brain natriuretic peptide and sildenafil in patients with pulmonary arterial hypertension
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DOI：
10.1378/chest.129.2.417
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发表时间：
2006-02-01
期刊：
影响因子：
9.6
通讯作者：
Farber, HW
中科院分区：
文献类型：
--
作者：
Klinger, JR;Thaker, S;Farber, HW
研究目的：脑利钠肽（BNP）在动物模型中可减轻缺氧性肺动脉高压，但其对肺动脉高压（PAH）患者急性血流动力学的影响尚不清楚。本研究的目的是确定人B型利钠肽是否是PAH患者安全有效的肺血管扩张剂，以及磷酸二酯酶抑制剂是否能增强肺血流动力学效应。设计：开放标签研究。设置：新英格兰三家三级护理医院的医学ICU。患者：13名连续接受右心导管插入术和肺血管扩张剂试验的成人患者，用于PAH的初步评价。患者吸入一氧化氮（iNO），静脉依前列醇，3小时输注BNP单独和1小时后，口服剂量的磷酸二酯酶-5抑制剂西地那非。结果：iNO和西地那非单独降低平均肺动脉压（mPAP）没有显着下降肺血管阻力（PVR）。依前列醇降低mPAP和PVR。BNP单独使用对肺血流动力学无显著影响，但西地那非联合BNP可降低mPAP和PVR，持续至停用BNP后6 h。西地那非+BNP（+/- SE）组的mPAP下降幅度大于西地那非单药治疗1小时后（44.6 +/- 3.8至40.6 +/- 3.9 min Hg，p = 0.027）。急性血管扩张反应，定义为mPAP降低> 10 mm Hg和终末mPAP < 40 mm Hg，在iNO组8例患者中为0例，依前列醇组13例患者中为1例，BNP组13例患者中为0例，西地那非+BNP组12例患者中为4例。BNP降低平均全身动脉压（5.6 +/- 2.8毫米汞柱），但对心输出量或全身血管resistance.Conclusions没有影响：3小时BNP输注并没有显着改善肺动脉高压患者的肺血流动力学，但耐受性良好，增强了西地那非的急性肺血管扩张作用。
Study objectives: Brain natriuretic peptide (BNP) blunts hypoxic pulmonary hypertension in animal models, but its acute hemodynamic effects in patients with pulmonary arterial hypertension (PAH) are not known. The aim of this study was to determine if human B-type natriuretic peptide is a safe and efficacious pulmonary vasodilator in patients with PAH and if the pulmonary hemodynamic effects are potentiated by phosphodiesterase inhibition.Design: Open-label study.Setting: Medical ICUs of three tertiary care hospitals in New England.Patients: Thirteen consecutive adult patients undergoing right-heart catheterization and a pulmonary vasodilator trial for the initial evaluation of PAH.Interventions: Patients were administered inhaled nitric, oxide (iNO), IV epoprostenol, and a 3-h infusion of BNP alone and 1 h after an oral dose of the phosphodiesterase-5 inhibitor sildenafil.Results: iNO and sildenafil alone decreased mean pulmonary artely pressure (mPAP) without a significant fall in pulmonary vascular resistance (PVR). Epoprostenol decreased both mPAP and PVR. BNP alone had no significant effect on pulmonary hemodynamics, but the combination of sildenafil plus BNP decreased mPAP and PVR for up to 6 h after stopping BNP. The decrease in mPAP with sildenafil plus BNP (+/- SE) was greater than after 1 h of sildenafil alone (44.6 +/- 3.8 to 40.6 +/- 3.9 min Hg, p = 0.027). An acute vasodilator response, defined as a decrease in mPAP > 10 mm Hg and end mPAP < 40 mm Hg, was seen in 0 of 8 patients with iNO, 1 of 13 patients with epoprostenol, 0 of 13 patients with BNP, and 4 of 12 patients with sildenafil plus BNP. BNP decreased mean systemic arterial pressure (5.6 +/- 2.8 mm Hg) but had no effect on cardiac output or systemic vascular resistance.Conclusions: A 3-h BNP infusion does not significantly improve pulmonary hemodynamics in most patients with PAH but is well tolerated and augments the acute pulmonary vasodilator effect of sildenafil.