Regulation of Placental Vascular Reactivity in Pregnancy-induced Hypertension
Information source: National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov processed this data on August 23, 2015
Link to the current ClinicalTrials.gov record.
Condition(s) targeted: Cardiovascular Diseases; Heart Diseases; Hypertension; Pregnancy Toxemias
Phase: N/A
Status: Completed
Sponsored by: National Heart, Lung, and Blood Institute (NHLBI)
Summary
To elucidate the role of an imbalance in vasodilator prostacyclin (PGI2) and vasoconstrictor
thromboxane (TxA2) in pregnancy-induced hypertension
Clinical Details
Study design: N/A
Detailed description:
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.
Eligibility
Minimum age: N/A.
Maximum age: N/A.
Gender(s): Male.
Criteria:
No eligibility criteria
Locations and Contacts
Additional Information
Related publications: Myatt L, Brewer AS, Brockman DE. The comparative effects of big endothelin-1, endothelin-1, and endothelin-3 in the human fetal-placental circulation. Am J Obstet Gynecol. 1992 Dec;167(6):1651-6. Myatt L. Control of vascular resistance in the human placenta. Placenta. 1992 Jul-Aug;13(4):329-41. Review. Eis AW, Mitchell MD, Myatt L. Endothelin transfer and endothelin effects on water transfer in human fetal membranes. Obstet Gynecol. 1992 Mar;79(3):411-5. Myatt L, Brewer AS, Langdon G, Brockman DE. Attenuation of the vasoconstrictor effects of thromboxane and endothelin by nitric oxide in the human fetal-placental circulation. Am J Obstet Gynecol. 1992 Jan;166(1 Pt 1):224-30. Myatt L, Langdon G, Brewer AS, Brockman DE. Endothelin-1-induced vasoconstriction is not mediated by thromboxane release and action in the human fetal-placental circulation. Am J Obstet Gynecol. 1991 Dec;165(6 Pt 1):1717-22. Jacobson RL, Brewer A, Eis A, Siddiqi TA, Myatt L. Transfer of aspirin across the perfused human placental cotyledon. Am J Obstet Gynecol. 1991 Oct;165(4 Pt 1):939-44. Myatt L, Brewer A, Brockman DE. The action of nitric oxide in the perfused human fetal-placental circulation. Am J Obstet Gynecol. 1991 Feb;164(2):687-92. Myatt L, Brockman DE, Langdon G, Pollock JS. Constitutive calcium-dependent isoform of nitric oxide synthase in the human placental villous vascular tree. Placenta. 1993 Jul-Aug;14(4):373-83.
Starting date: September 1987
Last updated: June 23, 2005
|
