Walsh S W
Perinatal Physiology Research Unit, University of Texas Medical School--Houston.
Obstet Gynecol. 1988 Feb;71(2):222-6.
Placentas obtained from women with preeclampsia produce more thromboxane, a potent vasoconstrictor, and less prostacyclin, a potent vasodilator, than normal. Although the factors responsible for this are not known, steroids are known to affect eicosanoid production, and the placenta is a rich source of progesterone and estradiol. If placental steroids contribute to the imbalance of increased thromboxane/decreased prostacyclin in preeclamptic placentas, then their placental production might also be abnormal. The following study was performed to see whether the placentas of preeclamptic women produce progesterone or estradiol abnormally. Fresh human term placentas were obtained immediately after delivery from normal and mild preeclamptic pregnancies. Whole placental tissues (350 mg) were incubated for three hours. Samples were collected and analyzed for progesterone and estradiol-17 beta by radioimmunoassay. Progesterone production was significantly higher in preeclamptic than in normal placentas without the addition of a precursor and with the addition of pregnenolone sulfate as a precursor, but not with the addition of pregnenolone alone. Both normal and preeclamptic placentas converted pregnenolone sulfate into progesterone as efficiently as they converted pregnenolone into progesterone. Estradiol production rates were similar in both preeclamptic and normal placentas, regardless of whether dehydroepiandrosterone sulfate was added as a precursor. These data indicate that placentas of women with mild preeclampsia produce more progesterone than normal, probably because they contain more pregnenolone sulfatase and larger stores of endogenous cholesterol. Higher concentrations of progesterone in the preeclamptic placenta could contribute to lower prostacyclin production because progesterone inhibits placental prostacyclin production.
与正常胎盘相比,子痫前期孕妇的胎盘产生更多的血栓素(一种强效血管收缩剂)和更少的前列环素(一种强效血管舒张剂)。尽管导致这种情况的因素尚不清楚,但已知类固醇会影响类花生酸的产生,而胎盘是孕酮和雌二醇的丰富来源。如果胎盘类固醇导致子痫前期胎盘血栓素增加/前列环素减少的失衡,那么它们在胎盘内的产生可能也不正常。进行以下研究以观察子痫前期孕妇的胎盘是否异常产生孕酮或雌二醇。在正常和轻度子痫前期妊娠分娩后立即获取新鲜的足月人胎盘。将整个胎盘组织(350毫克)孵育三小时。收集样本并通过放射免疫测定法分析孕酮和雌二醇-17β。在不添加前体以及添加硫酸孕烯醇酮作为前体的情况下,子痫前期胎盘的孕酮产生显著高于正常胎盘,但单独添加孕烯醇酮时则不然。正常胎盘和子痫前期胎盘将硫酸孕烯醇酮转化为孕酮的效率与将孕烯醇酮转化为孕酮的效率相同。无论是否添加硫酸脱氢表雄酮作为前体,子痫前期胎盘和正常胎盘的雌二醇产生率相似。这些数据表明,轻度子痫前期孕妇的胎盘产生的孕酮比正常胎盘多,可能是因为它们含有更多的孕烯醇酮硫酸酯酶和更多的内源性胆固醇储备。子痫前期胎盘孕酮浓度较高可能会导致前列环素产生减少,因为孕酮会抑制胎盘前列环素的产生。