Rich G F, Murphy G D, Roos C M, Johns R A
Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville 22908.
Anesthesiology. 1993 Jun;78(6):1028-35.
Inhaled nitric oxide (NO), an endothelium-derived relaxing factor, is a selective pulmonary vasodilator. The authors investigated whether the pulmonary vasodilation resulting from 20 ppm inhaled NO is related to the degree of pulmonary hypertension or affected by cardiopulmonary bypass (CPB) or the presence of intravenous nitrates.
In patients undergoing cardiac surgery (n = 20) or in whom the circulation was supported with a ventricular assist device (VAD; n = 5), the lungs were ventilated with 80% O2 and 20% N2 followed by the same gas concentrations containing 20 ppm NO for 6 min.
Inhaled NO decreased (P < 0.05) the pulmonary artery pressure from 36 +/- 3 to 29 +/- 2 mmHg and 32 +/- 2 to 27 +/- 1 mmHg, before and after CPB, respectively, and from 68 +/- 12 to 55 +/- 9 mmHg in patients with a VAD. Similarly, the pulmonary vascular resistance (PVR) decreased (P < 0.05) from 387 +/- 44 to 253 +/- 26 dyne.cm.s-5 and 260 +/- 27 to 182 +/- 18 dyne.cm.s-5, before and after CPB, respectively, and from 1,085 +/- 229 to 752 +/- 130 dyne.cm.s-5 in patients with a VAD. Central venous pressure, cardiac output, systemic hemodynamics, and blood gases did not change after inhalation of NO before or after CPB, whereas arterial oxygen tension, mixed venous hemoglobin saturation, and mean arterial pressure increased (P < 0.05) in patients supported with a VAD. All hemodynamic and laboratory data returned to control 6 min after discontinuation of NO. The decrease in PVR was proportional to baseline PVR (delta PVR = -0.45 PVRb + 39.9) before CPB. The pre- and post-CPB slopes were identical despite possible damage to the endothelium resulting from CPB and the post-CPB presence of intravenous nitroglycerin (17 of 20 patients).
This study demonstrates that 20 ppm inhaled NO is a selective pulmonary vasodilator in cardiac surgical patients before and after CPB and in patients in whom the circulation is supported with a VAD. Furthermore, NO-induced pulmonary vasodilation is proportional to PVRb and does not appear to be altered by CPB, the presence of a VAD, or infusion of nitrates.
吸入一氧化氮（NO）是一种内皮源性舒张因子，是一种选择性肺血管扩张剂。作者研究了吸入20 ppm NO所导致的肺血管扩张是否与肺动脉高压程度相关，或受体外循环（CPB）或静脉使用硝酸盐的影响。
在接受心脏手术的患者（n = 20）或使用心室辅助装置（VAD）支持循环的患者（n = 5）中，先使用80%氧气和20%氮气进行肺通气，然后使用含20 ppm NO的相同气体浓度通气6分钟。
吸入NO后，CPB前后肺动脉压力分别从36±3 mmHg降至29±2 mmHg和从32±2 mmHg降至27±1 mmHg，使用VAD的患者肺动脉压力从68±12 mmHg降至55±9 mmHg（P < 0.05）。同样，肺血管阻力（PVR）在CPB前后分别从387±44降至253±26 dyn·cm·s⁻⁵和从260±27降至182±18 dyn·cm·s⁻⁵，使用VAD的患者PVR从1085±229降至752±130 dyn·cm·s⁻⁵（P < 0.05）。CPB前后吸入NO后中心静脉压、心输出量、体循环血流动力学和血气均未改变，而使用VAD支持的患者动脉血氧分压、混合静脉血红蛋白饱和度和平均动脉压升高（P < 0.05）。停用NO 6分钟后，所有血流动力学和实验室数据均恢复至对照水平。CPB前PVR下降与基线PVR成比例（ΔPVR = -0.45PVRb + 39.9）。尽管CPB可能导致内皮损伤且CPB后有17/20患者静脉使用硝酸甘油，但CPB前后的斜率相同。
本研究表明，20 ppm吸入NO在CPB前后的心脏手术患者以及使用VAD支持循环的患者中是一种选择性肺血管扩张剂。此外，NO诱导的肺血管扩张与PVRb成比例，且似乎不受CPB、VAD的存在或硝酸盐输注的影响。
