Arnold-Aldea S A, Auslender R A, Parer J T
Cardiovascular Research Institute, University of California, San Francisco 94143-0132.
Am J Obstet Gynecol. 1991 Jul;165(1):185-90. doi: 10.1016/0002-9378(91)90248-p.
Treatment with prostaglandin synthesis inhibitors has been associated with oligohydramnios in the fetus. The presumed mechanism is a reduction in fetal renal blood flow. We examined the effect of meclofenamate administration on renal blood flow in chronically catheterized fetal sheep during normoxia and during moderate and severe hypoxia. Ten fetal sheep were made hypoxic twice at least 4 days after surgery: once in the presence and once in the absence of meclofenamate infusion. Renal blood flow and combined ventricular output were measured with radioactive microspheres. Prostaglandin synthesis blockade with meclofenamate caused no significant change in blood pressure, combined ventricular output, renal blood flow, or renal vascular resistance in either the normoxic or hypoxic animals. These data challenge the contention that prostaglandin activity protects the renal vascular bed of the fetus from vasoconstriction during hypoxia and they also do not support the hypothesis that prostaglandin synthesis inhibition causes oligohydramnios through reduction of fetal renal blood flow.
使用前列腺素合成抑制剂进行治疗与胎儿羊水过少有关。推测的机制是胎儿肾血流量减少。我们研究了在常氧、中度和重度缺氧期间，给予甲氯芬那酸对慢性插管胎羊肾血流量的影响。十只胎羊在手术后至少4天进行两次缺氧处理：一次在输注甲氯芬那酸的情况下，一次在未输注甲氯芬那酸的情况下。用放射性微球测量肾血流量和联合心室输出量。在常氧或缺氧动物中，甲氯芬那酸阻断前列腺素合成对血压、联合心室输出量、肾血流量或肾血管阻力均无显著影响。这些数据对前列腺素活性在缺氧期间保护胎儿肾血管床免受血管收缩的观点提出了挑战，同时也不支持前列腺素合成抑制通过减少胎儿肾血流量导致羊水过少的假说。
