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Although estrogen regulates important aspects of maternal cardiovascular physiology, the role of estrogen on uteroplacental and fetal blood flow is incompletely understood. This study tested the hypothesis that chronically suppressing endogenous estrogen production during the second half of baboon pregnancy alters uterine and fetal blood flow dynamics assessed by ultrasonography. Pregnant baboons were untreated or treated daily with the aromatase inhibitor letrozole or letrozole plus estradiol on days 100-160 of gestation (term = 184 days). Blood flow dynamics were determined by Doppler ultrasonography on day 60 and longitudinally between days 110 and 160 of gestation. Letrozole decreased maternal serum estradiol and estrone concentrations by 95% (P < 0.001). Fetal growth biometrical parameters increased (P < 0.001) between days 110 and 160 of gestation and were similar in untreated and letrozole-treated animals. Uterine, umbilical, and fetal middle cerebral artery pulsatility index and resistance index declined (P < 0.01) by 30-50% and uterine artery volume flow increased sixfold (P < 0.001) between days 60 and 160, but values were similar in untreated, letrozole-treated, and letrozole plus estradiol-treated baboons. Thus uterine and fetal artery blood flow indexes, uterine artery volume flow, and fetal growth were maintained at normal levels despite chronic estrogen suppression in the second half of baboon pregnancy. This suggests that elevated levels of endogenous estrogen are not required to maintain low impedance blood flow within the uteroplacental vascular bed during the second half of nonhuman primate pregnancy.

Objective: We have previously described placental oxygenation capacity as an index of placental function. The aim of this study was to utilize this test to evaluate placental gas exchange capacity in pre-eclampsia and fetal growth restriction (FGR). Study design: Two nested case-control studies were conducted between: (i) pre-eclamptic appropriate-for-gestational-age fetus (AGA) and non-pre-eclamptic AGA; and (ii) pre-eclamptic FGR and non-pre-eclamptic FGR based on gestational age match. Umbilical A-V gas differences were compared between groups. Results: Pre-eclamptic AGA was associated with smaller A-V pO2 and A-V pCO2 differences compared to non-pre-eclampsia (A-V pO2, 7.1±3.8 mm Hg vs. 11.3±5.9 mm Hg, P=0.001; A-V pCO2, 7.8±5.7 mm Hg vs. 10.7± 5.9 mm Hg, P=0.01). Pre-eclamptic FGR was associated with smaller A-V pO2 and A-V pCO2 differences compared to non-pre-eclampsia (A-V pO2, 6.6±3.1 mm Hg vs. 10.8±8.1 mm Hg, P<0.001; 6.7±4.5 mm Hg vs. 10.9±10.3 mm Hg, P=0.044). Pre-eclamptic FGR also had significantly lower venous pO2 but not arterial pO2 (Venous pO2, 20.3±6.3 mm Hg vs. 25.4±11.9 mm Hg, P=0.003). Conclusion: Pre-eclampsia decreases the placental oxygenation capacity as measured by the umbilical arterial-venous oxygen difference. [ABSTRACT FROM AUTHOR]