Hypertension Clinical Trial
To elucidate the role of an imbalance in vasodilator prostacyclin (PGI2) and vasoconstrictor thromboxane (TxA2) in pregnancy-induced hypertension
BACKGROUND:
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.
DESIGN NARRATIVE:
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.
The study completion date listed in this record was obtained from the "End Date" entered in
the Protocol Registration and Results System (PRS) record.
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