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Regulation of Placental Vascular Reactivity in Pregnancy-induced Hypertension

This study has been completed.
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00005208
First received: May 25, 2000
Last updated: February 26, 2016
Last verified: May 2000
  Purpose
To elucidate the role of an imbalance in vasodilator prostacyclin (PGI2) and vasoconstrictor thromboxane (TxA2) in pregnancy-induced hypertension

Condition
Cardiovascular Diseases
Heart Diseases
Hypertension
Pregnancy Toxemias

Study Type: Observational

Resource links provided by NLM:


Further study details as provided by National Heart, Lung, and Blood Institute (NHLBI):

Study Start Date: September 1987
Study Completion Date: July 1992
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.

The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.

  Eligibility

Ages Eligible for Study:   up to 100 Years   (Child, Adult, Senior)
Genders Eligible for Study:   Male
Accepts Healthy Volunteers:   No
Criteria
No eligibility criteria
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

No Contacts or Locations Provided
  More Information

Publications:
ClinicalTrials.gov Identifier: NCT00005208     History of Changes
Other Study ID Numbers: 1087  R01HL040029 
Study First Received: May 25, 2000
Last Updated: February 26, 2016
Health Authority: United States: Federal Government

Additional relevant MeSH terms:
Hypertension
Cardiovascular Diseases
Heart Diseases
Hypertension, Pregnancy-Induced
Pre-Eclampsia
Toxemia
Vascular Diseases
Pregnancy Complications
Infection

ClinicalTrials.gov processed this record on December 06, 2016