Ignite Creation Date:
2024-05-05 @ 11:07 AM
Last Modification Date:
2024-10-26 @ 9:04 AM
Study NCT ID:
NCT00005208
Status:
COMPLETED
Last Update Posted:
2016-02-29
First Post:
2000-05-25
Brief Title:
Regulation of Placental Vascular Reactivity in Pregnancy-induced Hypertension
Sponsor:
National Heart Lung and Blood Institute NHLBI
Organization:
National Heart Lung and Blood Institute NHLBI
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2000-05
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
To elucidate the role of an imbalance in vasodilator prostacyclin PGI2 and vasoconstrictor thromboxane TxA2 in pregnancy-induced hypertension
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 PGI2TxA2 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
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 PGI2TxA2 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
Study Oversight
Has Oversight DMC:
Is a FDA Regulated Drug?:
Is a FDA Regulated Device?:
Is an Unapproved Device?:
Is a PPSD?:
Is a US Export?:
Is an FDA AA801 Violation?:
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL040029 | NIH | None | httpsreporternihgovquickSearchR01HL040029 |