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吸入一氧化氮对接受机械循环辅助的患者体循环血流量和心室充盈压的影响。

Influence of inhaled nitric oxide on systemic flow and ventricular filling pressure in patients receiving mechanical circulatory assistance.

作者信息

Hare J M, Shernan S K, Body S C, Graydon E, Colucci W S, Couper G S

机构信息

Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Md, USA.

出版信息

Circulation. 1997 May 6;95(9):2250-3. doi: 10.1161/01.cir.95.9.2250.

DOI:10.1161/01.cir.95.9.2250
PMID:9142001
Abstract

BACKGROUND

In patients with left ventricular (LV) dysfunction, inhaled nitric oxide (NO) decreases pulmonary vascular resistance (PVR) but causes a potentially clinically significant increase in left atrial pressure (LAP). This has led to the suggestion that inhaled NO may reach the coronary circulation and have a negative inotropic effect. This study tested an alternative hypothesis that LAP increases because of volume shifts to the pulmonary venous compartment caused by NO-induced selective pulmonary vasodilation.

METHODS AND RESULTS

The Thermo Cardiosystems Heartmate is an LV assist device (LVAD) that can be set (by controlling pump rate) to deliver fixed or variable systemic blood flow. Eight patients (between 1 and 11 days after LVAD implantation) were administered inhaled NO (20 and 40 ppm for 10 minutes), and LAP, systemic flow, and pulmonary arterial pressure were measured in both fixed and variable pump flow modes. In both modes, inhaled NO lowered PVR (by 25 +/- 6% in the fixed mode, P < .001, and by 21 +/- 5% in the variable mode, P < .003). With fixed pump flow, LAP rose from 12.5 +/- 1.2 to 15.1 +/- 1.4 mm Hg (P < .008). In the variable flow mode, LAP did not increase and the assist device output rose from 5.3 +/- 0.3 to 5.7 +/- 0.3 L/min (P < .008).

CONCLUSIONS

A selective reduction in PVR by inhaled NO can increase LAP if systemic flow cannot increase. These data support the hypothesis that with LV failure, inhaled NO increases LAP by increasing pulmonary venous volume and demonstrate that inhaled NO has beneficial hemodynamic effects in LVAD patients.

摘要

背景

在左心室(LV)功能不全的患者中,吸入一氧化氮(NO)可降低肺血管阻力(PVR),但会导致左心房压力(LAP)出现可能具有临床意义的升高。这使得人们认为吸入的NO可能进入冠状动脉循环并产生负性肌力作用。本研究检验了另一种假设,即LAP升高是由于NO诱导的选择性肺血管舒张导致容量转移至肺静脉腔所致。

方法与结果

热控心血管系统Heartmate是一种左心室辅助装置(LVAD),可通过控制泵速设置为输送固定或可变的全身血流量。8例患者(LVAD植入后1至11天)吸入NO(20和40 ppm,持续10分钟),并在固定和可变泵流量模式下测量LAP、全身血流量和肺动脉压力。在两种模式下,吸入NO均降低了PVR(固定模式下降低25±6%,P<.001;可变模式下降低21±5%,P<.003)。在固定泵流量时,LAP从12.5±1.2 mmHg升至15.1±1.4 mmHg(P<.008)。在可变流量模式下,LAP未升高,辅助装置输出从5.3±0.3 L/min升至5.7±0.3 L/min(P<.008)。

结论

如果全身血流量不能增加,吸入NO选择性降低PVR可使LAP升高。这些数据支持了以下假设,即左心室衰竭时,吸入NO通过增加肺静脉容量使LAP升高,并表明吸入NO对LVAD患者具有有益的血流动力学效应。

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