Regulation of Placental Vascular Reactivity in Pregnancy-Induced Hypertension
To elucidate the role of an imbalance in vasodilator prostacyclin (PGI2) and vasoconstrictor thromboxane (TxA2) in pregnancy-induced hypertension
|Study Design:||Observational Model: Natural History|
|Study Start Date:||September 1987|
|Estimated Study Completion Date:||July 1992|
Pregnancy-induced hypertension (PIH) is associated with increased fetal and neonatal morbidity and mortality possibly resulting from hypoxia in utero. The primary pathology of PIH involves a reduction in uteroplacental blood flow but modern imaging techniques have now shown that increased impedance of the fetal-placental circulation and hence reduced blood flow can also be found in PIH. This may represent a direct effect of hypoxia or be a fetal adaptation to increase placental oxygen extraction to relieve hypoxia. The fetal-placental circulation is regulated by humoral agents and vascular pressure. An imbalance of vasodilator prostacyclin (PGI2) and vasoconstrictor thromboxane (TxA2) production is reported to underlie the vasoconstriction seen in PIH.
The study resulted from the 1986 release of a Request for Applications for Research on Hypertension in Pregnancy by the National Heart, Lung, and Blood Institute and the National Institute of Child Health and Human Development.
The fetal-placental circulations of perfused human placental cotyledons from normotensive and pregnancy-induced hypertensive pregnancies were used to determine if an imbalance in PGI2/TxA2 production existed and its relationship to the responses of the fetal-placental circulation to vasoconstriction. Studies were also conducted on the effects of hypocalcemia and hypomagnesemia, hypoxia, and drugs.