Karlsson K, Ljungblad U, Lundgren Y
Am J Obstet Gynecol. 1982 Apr 15;142(8):1039-44. doi: 10.1016/0002-9378(82)90790-6.
An experimental study on pregnant rats was undertaken to explore whether renal hypertension interferes with uteroplacental blood supply and fetal weight. Renal hypertension was induced by standardized clamping of the left renal artery. Two days before expected delivery, blood flow to the reproductive organs was determined by microsphere technique in normal control rats, rats with short-standing renal hypertension induced early in pregnancy, and rats with established renal hypertension induced 4 weeks before pregnancy. Myometrial and placental blood supply was considerably reduced in renal hypertensive rats compared to that in normotensive pregnant rats, with the reduction in placental blood flow being as much as 68% in rats with established renal hypertension. Nevertheless, there was no reduction in fetal weights, placental weights, or number of fetuses in the litters. These findings suggest that the nutritional blood supply of the placenta normally has a considerable overcapacity, perhaps a necessary safety margin so that the fetus can manage the circulatory demands associated with delivery. If hypertension causes intrauterine growth retardation only by means of reduced placental blood flow, this reduction in flow obviously must be considerable.
进行了一项关于妊娠大鼠的实验研究，以探讨肾性高血压是否会干扰子宫胎盘血液供应和胎儿体重。通过标准化夹闭左肾动脉诱导肾性高血压。在预期分娩前2天，采用微球技术测定正常对照大鼠、妊娠早期诱发短期肾性高血压的大鼠以及妊娠前4周诱发已形成肾性高血压的大鼠生殖器官的血流量。与正常血压妊娠大鼠相比，肾性高血压大鼠的子宫肌层和胎盘血液供应明显减少，在已形成肾性高血压的大鼠中，胎盘血流量减少多达68%。然而，胎仔的胎儿体重、胎盘重量或胎儿数量并未减少。这些发现表明，胎盘的营养性血液供应通常具有相当大的过剩能力，这可能是一个必要的安全边际，以便胎儿能够应对与分娩相关的循环需求。如果高血压仅通过减少胎盘血流量导致宫内生长受限，那么这种血流量的减少显然必须相当大。
