Theissen J L, Loick H M, Traber L D, Herndon D N, Traber D L
Department of Anesthesiology, University of Texas Medical Branch, Galveston.
J Burn Care Rehabil. 1992 Nov-Dec;13(6):623-7. doi: 10.1097/00004630-199211000-00003.
The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.
在长期植入仪器并麻醉的绵羊（空气中含1.7%氟烷）（n = 8）中评估吸入一氧化碳对肺血管的直接收缩作用。通过双腔管将2%的一氧化碳交替施加于每只动物的左肺或右肺8分钟，将其反应与基线值进行比较。诱导产生的碳氧血红蛋白水平（65%）导致心输出量、肺动脉压、每搏量指数和心率增加。全身血管阻力降低，肺血管阻力和平均动脉压未改变。无论哪侧肺暴露于一氧化碳，压力和流量的变化都是相同的。在测试期间未观察到血液从一侧肺分流至另一侧。我们得出结论，一氧化碳没有直接的肺血管收缩作用。肺动脉压升高是混合静脉血氧含量降低（缺氧性肺血管收缩的刺激因素）和心输出量增加的结果。
