Saltz S B, Beller G A, Giamber S R, Alpert J S
Aviat Space Environ Med. 1976 Feb;47(2):129-32.
Hemodynamics were studied in seven conscious dogs during acute hypobaric stress at 14,000 ft simulated altitude. Silastic catheters were chronically implanted in the pulmonary artery, left atrium, and aorta. Pulmonary and central aortic pressures, cardiac output, and pulmonary blood volume were determined under conditions of normoxia and acute hypoxia in a hypobaric chamber maintained at 446 mm Hg pressure (14,000 ft). Altitude resulted in significant increases in heart rate, cardiac output, pulmonary blood volume, and pulmonary artery pressure. Left atrial pressure and calculated systemic vascular resistance decreased during hypobaric hypoxia while stroke volume, stroke work index, arterial pressure and pulmonary vascular resistance remained unchanged. Arterial blood PO2 decreased markedly at altitude, and all animals hyperventilated with resultant systemic hypocarbic alkalosis. The combination of elevated pulmonary arterial pressure and increased pulmonary blood volume may by an etiologic factor in the development of high-altitude pulmonary edema.
在模拟海拔14000英尺的急性低压应激期间，对7只清醒犬的血流动力学进行了研究。将硅橡胶导管长期植入肺动脉、左心房和主动脉。在保持压力为446毫米汞柱（14000英尺）的低压舱内，于常氧和急性缺氧条件下测定肺和中心主动脉压力、心输出量及肺血容量。海拔导致心率、心输出量、肺血容量和肺动脉压力显著增加。在低压缺氧期间，左心房压力和计算得出的体循环血管阻力降低，而每搏量、每搏作功指数、动脉压和肺血管阻力保持不变。海拔时动脉血氧分压显著降低，所有动物均出现过度通气，导致全身性低碳酸性碱中毒。肺动脉压力升高和肺血容量增加的联合作用可能是高原肺水肿发生发展中的一个病因因素。
