Anderson D F, Borst C G, Faber J J
Department of Physiology, School of Medicine, Oregon Health Sciences University, Portland 97201-3098, USA.
Eur J Obstet Gynecol Reprod Biol. 1995 Dec;63(2):175-9. doi: 10.1016/0301-2115(95)02232-5.
It is known that a week-long infusion of angiotensin into fetal sheep produces polyhydramnios. The purpose of the present experiments was to determine whether an increased osmotic force across the placental barrier could account for the excess transfer of water. Six fetuses with indwelling catheters were infused with angiotensin-I and one with angiotensin-II; all, except one fetus in the first group, developed gross polyhydramnios. None of the transplacental concentration differences of the small plasma solutes Na+, Cl-, HCO3-, K+, urea, or glucose showed a demonstrable change and the same was true of the transplacental difference in freezing point osmolality and for the transplacental difference in plasma protein concentration. It is concluded that the infusion of angiotensin at a low dose rate is a reliable protocol for producing polyhydramnios. However, the present findings lend no support to the hypothesis that a primary change in transplacental osmotic force is the cause of the increased transplacental water transfer in this form of polyhydramnios. Alternative hypotheses are discussed in the light of recent discoveries.
已知向胎羊体内持续输注一周的血管紧张素会导致羊水过多。本实验的目的是确定胎盘屏障渗透压升高是否能解释水分的过度转移。给6只留置导管的胎儿输注血管紧张素-I，给1只胎儿输注血管紧张素-II；除第一组中的1只胎儿外，所有胎儿均出现明显的羊水过多。血浆中小溶质Na+、Cl-、HCO3-、K+、尿素或葡萄糖的跨胎盘浓度差异均未显示出明显变化，冰点渗透压的跨胎盘差异以及血浆蛋白浓度的跨胎盘差异也是如此。得出的结论是，以低剂量率输注血管紧张素是产生羊水过多的可靠方法。然而，目前的研究结果并不支持以下假设：跨胎盘渗透压的原发性变化是这种形式的羊水过多中跨胎盘水分转移增加的原因。根据最近的发现讨论了其他假设。
