Abman S H, Accurso F J, Wilkening R B, Meschia G
Department of Pediatrics, University of Colorado School of Medicine, Denver 80262.
Am J Physiol. 1987 Oct;253(4 Pt 2):H941-8. doi: 10.1152/ajpheart.1987.253.4.H941.
To determine the effects of duration of hypoxia on fetal pulmonary blood flow and vasoreactivity, we studied the response of the fetal pulmonary vascular bed before, during, and after prolonged (2-h) and more brief (30-min) exposures to acute hypoxia in 19 chronically instrumented unanesthetized fetal lambs. Left pulmonary arterial blood flow was measured by an electromagnetic flow transducer. Fetal PO2 was lowered by delivering 10-12% O2 to the ewe. During 2-h periods of hypoxia left pulmonary arterial blood flow decreased, and main pulmonary arterial and pulmonary vascular resistance increased. The increase in pulmonary vascular resistance was sustained throughout the 2-h period of hypoxia. After the return of the ewe to room air breathing, pulmonary vascular resistance remained elevated for at least 1 h despite the rapid correction of hypoxemia and in the absence of acidemia. In contrast, after 30 min of hypoxia, left pulmonary arterial blood flow, pulmonary arterial pressure, and pulmonary vascular resistance returned to base-line values rapidly with the termination of hypoxia. The persistent pulmonary hypoperfusion after 2 h of hypoxia was attenuated by alpha-adrenergic blockade and was characterized by a blunted vasodilatory response to increases in fetal PO2. When fetal PO2 was elevated during the posthypoxia period in the presence of alpha-blockade, pulmonary blood flow still remained unresponsive to increases in fetal PO2. We conclude that 2-h periods of acute hypoxia can decrease fetal pulmonary vasoreactivity, and we speculate that related mechanisms may contribute to the failure of the normal adaptation of the pulmonary circulation at birth.
为了确定缺氧持续时间对胎儿肺血流量和血管反应性的影响，我们对19只长期植入仪器且未麻醉的胎羊进行了研究，观察了在长时间（2小时）和更短时间（30分钟）急性缺氧暴露之前、期间和之后胎儿肺血管床的反应。通过电磁流量传感器测量左肺动脉血流量。通过向母羊输送10 - 12%的氧气来降低胎儿的氧分压。在2小时的缺氧期间，左肺动脉血流量减少，主肺动脉和肺血管阻力增加。肺血管阻力的增加在整个2小时的缺氧期间持续存在。母羊恢复呼吸室内空气后，尽管低氧血症迅速得到纠正且不存在酸中毒，但肺血管阻力至少在1小时内仍保持升高。相比之下，在缺氧30分钟后，随着缺氧的终止，左肺动脉血流量、肺动脉压和肺血管阻力迅速恢复到基线值。缺氧2小时后持续的肺灌注不足通过α - 肾上腺素能阻滞得以减轻，其特征是对胎儿氧分压升高的血管舒张反应减弱。当在α - 阻滞剂存在的情况下，在缺氧后阶段胎儿氧分压升高时，肺血流量对胎儿氧分压的升高仍无反应。我们得出结论，2小时的急性缺氧可降低胎儿肺血管反应性，并且我们推测相关机制可能导致出生时肺循环正常适应的失败。
