Putensen C, Räsänen J, López F A, Downs J B
Department of Anesthesiology, University of South Florida, College of Medicine, Tampa 33612-4799.
Chest. 1994 Nov;106(5):1563-9. doi: 10.1378/chest.106.5.1563.
The present study was designed to evaluate if continuous positive airway pressure (CPAP) augments the effect of nitric oxide (NO) inhalation on matching between ventilation and perfusion (VA/Q) during acute lung injury.
Prospective, randomized study.
A research laboratory at a university medical center.
Ten anesthetized mongrel dogs with oleic acid-induced lung injury.
Zero or 40 parts per million of NO in the inspiratory gas, with and without 10 cm H2O CPAP in random order.
Gas exchange was assessed by estimating the VA/Q distributions using the multiple inert gas elimination technique. Application of CPAP decreased blood flow to shunt units by 26 +/- 2 percent (mean +/- SD) and increased the fraction of cardiac output to normal VA/Q units (VA/Q ratio of 0.1 to 10) by 26 +/- 2 percent (p < 0.05). Inhalation of NO during CPAP accounted for a further 10 +/- 2 percent decrease in the blood flow to shunt units and an 8 +/- 2 percent increase in the fraction of the cardiac output to normal VA/Q units (p < 0.05). Inhalation of NO alone had no significant effect on the VA/Q distributions. Inhalation of NO decreased mean transmural pulmonary artery pressure (Ppatm) both without (Ppatm from 30 +/- 2 to 23 +/- 2 mm Hg; PVR from 323 +/- 44 to 228 +/- 43 dynes.s .cm-5; p < 0.05) and with CPAP (Ppatm from 25 +/- 2 to 20 +/- 2 mm Hg; PVR from 255 +/- 30 to 173 +/- 31 dynes.s.cm-5; p < 0.05).
Although pulmonary vascular resistance can be lowered with NO inhalation alone, recruitment of gas exchange units with CPAP is necessary to produce a beneficial effect of NO inhalation on VA/Q matching and oxygenation. When recruitment of gas exchange units with CPAP brings gaseous NO in contact with enough pulmonary blood vessels, NO-induced vasodilation will augment VA/Q matching by a steal mechanism.
本研究旨在评估持续气道正压通气（CPAP）是否能增强一氧化氮（NO）吸入对急性肺损伤期间通气与灌注匹配（VA/Q）的影响。
前瞻性随机研究。
大学医学中心的研究实验室。
十只油酸诱导肺损伤的麻醉杂种犬。
吸入气体中一氧化氮浓度为零或百万分之40，随机顺序施加或不施加10 cm H2O的CPAP。
采用多惰性气体排除技术评估VA/Q分布来评估气体交换。施加CPAP使分流单位的血流减少26±2%（均值±标准差），使心输出量流向正常VA/Q单位（VA/Q比值为0.1至10）的比例增加26±2%（p<0.05）。在CPAP期间吸入NO使分流单位的血流进一步减少10±2%，使心输出量流向正常VA/Q单位的比例增加8±2%（p<0.05）。单独吸入NO对VA/Q分布无显著影响。吸入NO可降低平均跨壁肺动脉压（Ppatm），无论有无CPAP均如此（无CPAP时，Ppatm从30±2降至23±2 mmHg；肺血管阻力从323±44降至228±43 dynes·s·cm-5；p<0.05；有CPAP时，Ppatm从25±2降至20±2 mmHg；肺血管阻力从255±30降至173±31 dynes·s·cm-5；p<0.05）。
虽然单独吸入NO可降低肺血管阻力，但要使吸入NO对VA/Q匹配和氧合产生有益作用，必须通过CPAP募集气体交换单位。当通过CPAP募集气体交换单位使气态NO与足够的肺血管接触时，NO诱导的血管舒张将通过窃取机制增强VA/Q匹配。
