Cheney F W, Pavlin J, Ferens J, Allen D
J Thorac Cardiovasc Surg. 1978 Oct;76(4):473-8.
The effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.
急性肺动脉高压对经肺动静脉分流的心脏输出量分数的影响已在犬类中进行研究，这可能是肺栓塞后缺氧的一个原因。通过用聚苯乙烯微球栓塞肺血管床，使肺动脉压力比对照值增加两倍，然后增加四倍。通过注入下腔静脉的50微米放射性标记微球经肺循环进入体循环血管床的分数来定量测定动静脉分流。当FiO2为1时，肺微栓塞时通过直径50微米或更大的肺动静脉连接的肺血流量分数没有增加。当FiO2为0.21时，肺动脉压力升高时动静脉分流分数有小幅增加。用氧技术测量的生理分流并未因肺栓塞而增加，但总静脉混合显著上升。死后肺水重量测量表明存在肺水肿。我们得出结论，在犬肺中肺微栓塞后，解剖学上的动静脉分流通道几乎没有生理意义。肺微栓塞后立即缺氧的主要原因是通气/灌注失衡，可能是由肺水肿引起的。
