| Endothelin and the regulation of uterine and placental perfusion in hypoxia-induced fetal growth restriction. | |
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MedLine Citation:
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PMID: 14706678 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: Normal placental function is dependent on maintenance of uteroplacental perfusion. Endothelin, a potent vasoconstrictor, is produced in and is active in the uteroplacental vasculature. The purpose of this study was to determine the role of endothelin in the regulation of uteroplacental perfusion under normal conditions, and in hypoxia-induced fetal growth restriction. METHODS: Timed-pregnant Sprague-Dawley rats, outfitted with arterial catheters, were maintained in either a normoxic or a normobaric hypoxic (12% oxygen) atmosphere from day 18 to 21 of gestation. During this time, the endothelin receptor A antagonist, A-127722, or its vehicle was administered. Regional blood flow was determined on gestational day 21 using 57Co-labeled microspheres. Data were analyzed by analysis of variance with statistical significance accepted at P<.05. RESULTS: Both placental and uterine placental bed perfusion were significantly decreased by hypoxia and returned to normal values with the endothelin antagonist (P<.01 and P<.05, respectively). Fetal weights were significantly lower in the hypoxic group (P<.001) and restored to control levels by the antagonist. CONCLUSION: In the rat, endothelin contributes little to the regulation of uteroplacental perfusion under normal conditions. Hypoxia results in a decrease in perfusion of the uteroplacental bed and of the placenta, and perfusion in both of these beds is normalized by endothelin A receptor antagonism. We conclude that endothelin plays a primary role in the pathophysiology of hypoxia-induced fetal growth restriction by reducing uteroplacental perfusion. |
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Authors:
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Larry G Thaete; Elizabeth R Dewey; Mark G Neerhof |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of the Society for Gynecologic Investigation Volume: 11 ISSN: 1071-5576 ISO Abbreviation: J. Soc. Gynecol. Investig. Publication Date: 2004 Jan |
Date Detail:
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Created Date: 2004-01-06 Completed Date: 2004-03-11 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9433806 Medline TA: J Soc Gynecol Investig Country: United States |
Other Details:
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Languages: eng Pagination: 16-21 Citation Subset: IM |
Affiliation:
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Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. lthaete@enh.org |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Flow Velocity Blood Pressure Cobalt Radioisotopes Endothelin-1 / physiology* Female Fetal Growth Retardation / etiology*, physiopathology* Fetal Hypoxia / complications* Fetus / blood supply Gestational Age Kidney / blood supply Microspheres Oxygen / administration & dosage Placenta / blood supply* Pregnancy Pyrrolidines / pharmacology Rats Rats, Sprague-Dawley Receptor, Endothelin A / antagonists & inhibitors Uterus / blood supply* |
| Grant Support | |
ID/Acronym/Agency:
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HD01484/HD/NICHD NIH HHS; HD34777/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/A 127722; 0/Cobalt Radioisotopes; 0/Endothelin-1; 0/Pyrrolidines; 0/Receptor, Endothelin A; 7782-44-7/Oxygen |
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