Pearl R G, Siegel L C
Department of Anesthesia, Stanford University Medical Center, California 94305-5117.
Anesthesiology. 1992 Jan;76(1):106-12. doi: 10.1097/00000542-199201000-00016.
Pulmonary capillary pressure (Ppc) is dependent upon left atrial pressure, pulmonary venous resistance, and cardiac output. The effects of pulmonary vasodilators on Ppc will therefore depend upon any alterations in the longitudinal distribution of pulmonary vascular resistance (precapillary [arterial] and postcapillary [venous] components). We therefore studied the effects of two pulmonary vasodilators (prostaglandin E1 and hydralazine) on Ppc and the longitudinal distribution of pulmonary vascular resistance. Pulmonary hypertension was produced in sheep by the continuous administration of the thromboxane A2-mimetic U46619. Ppc was measured by analysis of pulmonary artery occlusion pressure decay curves. U46619 increased Ppc by 9 mmHg and increased both the arterial and venous components of pulmonary vascular resistance. Subsequent administration of prostaglandin E1 decreased Ppc by 5 mmHg and decreased both the arterial and venous components of pulmonary vascular resistance (by 50 and 69% respectively). Hydralazine produced smaller decreases in the arterial and venous components of pulmonary vascular resistance (by 35 and 49% respectively) and did not significantly reduce Ppc. We conclude that prostaglandin E1 but not hydralazine is effective in decreasing Ppc in this experimental model of pulmonary hypertension.
肺毛细血管压（Ppc）取决于左心房压力、肺静脉阻力和心输出量。因此，肺血管扩张剂对Ppc的影响将取决于肺血管阻力（毛细血管前[动脉]和毛细血管后[静脉]成分）纵向分布的任何改变。因此，我们研究了两种肺血管扩张剂（前列腺素E1和肼屈嗪）对Ppc和肺血管阻力纵向分布的影响。通过持续给予血栓素A2模拟物U46619在绵羊中诱导肺动脉高压。通过分析肺动脉闭塞压衰减曲线来测量Ppc。U46619使Ppc升高9 mmHg，并增加了肺血管阻力的动脉和静脉成分。随后给予前列腺素E1使Ppc降低5 mmHg，并降低了肺血管阻力的动脉和静脉成分（分别降低50%和69%）。肼屈嗪使肺血管阻力的动脉和静脉成分降低幅度较小（分别降低35%和49%），且未显著降低Ppc。我们得出结论，在这个肺动脉高压实验模型中，前列腺素E1可有效降低Ppc，而肼屈嗪则无效。
