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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 clays 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 six-fold (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. uterus; fetus doi:10.1152/ajpheart.00611.2009

Aims: To test if an isolated finding of low-normal amniotic fluid index (AF1) in the early third trimester in low-risk patients is associated with adverse perinatal outcomes. Methods: Retrospective cohort study with uncomplicated singleton pregnancies that had ultrasound studies between 28.0 and 31.9 weeks' gestation. Two cohorts with AFI 8.0-11.9 cm (low-normal, LN) and AFI 12.0-19.9 cm (mid-normal, MN) were compared. Results: Patients with LN-AFI (n=99) were more likely to have early (<34 weeks) and late (<37 weeks) preterm birth (PTB) (relative risk 4.2 and 2.4, respectively) and a small for gestational age (SGA) infant (relative risk 1.8) than MN-AFI (n=834), corresponding to a higher NICU admission rate (relative risk 2.5). The risk of "spontaneous" PTB (preterm labor and rupture of membranes) did not differ between the cohorts, whereas the risk of "indicated" PTB (maternal or fetal indications) was significantly increased in LN-AFI. The incidence of abnormal antepartum testing, stillbirth, preeclampsia, placental abruption, fetal intolerance to labor, emergency cesarean delivery, umbilical artery pH <7.0, Apgar scores <7 at 5 min, and neonatal death was not increased in patients with LN-AFI. Conclusion: Low-normal AFI in the early third trimester increases the risk for subsequent delivery of an SGA infant and indicated PTB. [ABSTRACT FROM AUTHOR]

The present study was conducted to determine the impact of suppressing trophoblast remodeling of the uterine spiral arteries by prematurely elevating estrogen levels in the first trimester of baboon pregnancy on uterine and umbilical blood flow dynamics. Uteroplacental blood flow was assessed by Doppler ultrasonography after acute administration of saline (basal state) and serotonin on days 60, 100, and 160 of gestation (term: 184 days) to baboons in which uterine spiral artery remodeling had been suppressed by the administration of estradiol on days 25-59 of gestation. Maternal blood pressure in the basal state was increased (P < 0.01), and uterine artery diastolic notching and the umbilical artery pulsatility index and systolic-to-diastolic ratio, reflecting downstream flow impedance, were increased (P < 0.01) after serotonin administration on day 160, but not earlier, in baboons treated with estradiol in early gestation. These changes in uteroplacental flow dynamics in serotonin-infused, estradiol-treated animals were accompanied by a decrease (P < 0.05) in uterine and umbilical artery volume flow and fetal bradycardia. The results of this study show that suppression of uterine artery remodeling by advancing the rise in estrogen from the second trimester to the first trimester disrupted uteroplacental blood flow dynamics and fetal homeostasis after vasochallenge late in primate pregnancy.