Frostell C G, Blomqvist H, Hedenstierna G, Lundberg J, Zapol W M
Department of Anaesthesia and Intensive Care, Danderyd Hospital, Sweden.
Anesthesiology. 1993 Mar;78(3):427-35. doi: 10.1097/00000542-199303000-00005.
Nitric oxide (NO), an endothelium-derived relaxing factor, acts as a local vasodilator. The authors examined the effects of NO on pulmonary and systemic circulation in human volunteers.
Nine healthy adults were studied awake while breathing 1) air, 2) 12% O2 in N2, 3) followed by the same mixture of O2 and N2 containing 40 ppm of NO. Pulmonary artery and radial artery pressures were monitored.
The PaO2 decreased from 106 +/- 4 (mean +/- standard error of the mean) while breathing air (21% O2) to 47 +/- 2 mmHg after 6 min of breathing 12% O2. Concomitantly, the pulmonary artery mean pressure (PAP) increased from 14.7 +/- 0.8 mmHg to 19.8 +/- 0.9 mmHg, and the cardiac output (CO) increased from 6.1 +/- 0.4 to 7.7 +/- 0.6 L/min. After adding 40 ppm NO to the inspired gas while maintaining the FIO2 at 0.12, the PAP decreased (P < 0.01, by analysis of variance) to the level when breathing air while the PaO2 and PaCO2 were unchanged. The dilation (or recruitment) of pulmonary vessels produced by inhaling NO during hypoxia was not accompanied by any alteration in the systemic vascular resistance or mean arterial pressure (MAP). The authors also examined the effects of inhaling NO while breathing air. Breathing 40 ppm NO in 21% O2 for 6 min produced no significant changes of PAP, CO, PaO2, MAP, or central venous pressure. Plasma endothelinlike immunoreactivity concentrations did not change either during hypoxia or hypoxia with NO inhalation.
Inhalation of 40 ppm NO selectively induced pulmonary vasodilation and reversed hypoxic pulmonary vasoconstriction in healthy humans without causing systemic vasodilation.
一氧化氮（NO）是一种内皮源性舒张因子，作为局部血管扩张剂发挥作用。作者研究了NO对人类志愿者肺循环和体循环的影响。
对9名健康成年人进行清醒状态下的研究，他们分别呼吸1）空气、2）氮气中12%的氧气、3）随后呼吸含有40 ppm NO的相同氧气和氮气混合物。监测肺动脉和桡动脉压力。
呼吸空气（21%氧气）时，动脉血氧分压（PaO2）为106±4（平均值±平均标准误差），呼吸12%氧气6分钟后降至47±2 mmHg。同时，肺动脉平均压（PAP）从14.7±0.8 mmHg升至19.8±0.9 mmHg，心输出量（CO）从6.1±0.4升至7.7±0.6 L/分钟。在维持吸入氧分数（FIO2）为0.12的情况下，向吸入气体中添加40 ppm NO后，PAP下降（方差分析，P<0.01）至呼吸空气时的水平，而PaO2和动脉血二氧化碳分压（PaCO2）未改变。缺氧时吸入NO所产生的肺血管扩张（或再灌注）并未伴随体循环血管阻力或平均动脉压（MAP）的任何改变。作者还研究了呼吸空气时吸入NO的影响。在21%氧气中呼吸40 ppm NO 6分钟，PAP、CO、PaO2、MAP或中心静脉压均无显著变化。低氧期间或低氧合并吸入NO期间，血浆内皮素样免疫反应性浓度均未改变。
吸入40 ppm NO可选择性地诱导健康人肺血管扩张并逆转低氧性肺血管收缩，而不会引起体循环血管扩张。
