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BOR - Papers in Press, published online ahead of print May 17, 2006.
Biol Reprod 2006, 10.1095/biolreprod.106.051607
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BIOLOGY OF REPRODUCTION 75, 518–523 (2006)
DOI: 10.1095/biolreprod.106.051607
© 2006 by the Society for the Study of Reproduction, Inc.

Research Article

Reactivity of Human Placental Chorionic Plate Vessels from Pregnancies Complicated by Intrauterine Growth Restriction (IUGR)1

Mark Wareing 2, Susan L. Greenwood , Gregor K. Fyfe , and Philip N. Baker 

Division of Human Development, Maternal and Fetal Health Research Center, The University of Manchester, St. Mary's Hospital, Manchester M13 0JH, United Kingdom

ABSTRACT

A successful pregnancy is dependent on liberal placental perfusion via the maternal and fetal circulations. Doppler waveform analyses of umbilical arteries suggest increased resistance to flow in the fetoplacental circulation of pregnancies complicated by intrauterine growth restriction (IUGR). Neither the site nor the mediators responsible for this altered vascular reactivity are known, to date. In placentas in normal pregnancy, reduced oxygenation promotes contraction of the in vitro-perfused placental cotyledon and modulates agonist-induced contraction of chorionic plate arteries and veins. Placental oxygenation has also been suggested to be reduced in IUGR. We tested the hypothesis that oxygen tension could directly modify placental chorionic plate vessel vasoreactivity in IUGR. Small arteries and veins from the chorionic plate were dissected from biopsies from placentas of pregnancies complicated by IUGR and were studied using parallel wire myography. Vasoconstriction at 20%, 7%, and 2% oxygen was assessed utilizing the thromboxane mimetic U46619. Experiments were also performed in the presence of 4-aminopyridine (4AP), a blocker of voltage-gated potassium channels. Increased oxygenation reduced venous vasoconstriction but did not modify arterial vasoconstriction. 4AP increased basal tone in arteries and veins. We suggest that venoconstriction in response to hypoxia may provide a mechanism for increased fetoplacental vascular resistance associated with IUGR.

placenta, pregnancy

FOOTNOTES

1 Supported by Tommy's the baby charity (Maternal and Fetal Health Research Center) and by a British Heart Foundation Intermediate Clinical Research Fellowship (M.W.; grant FS/03/051).

2 Correspondence: Mark Wareing, Division of Human Development, Maternal and Fetal Health Research Center, The University of Manchester, St. Mary's Hospital, Hathersage Road, Manchester M13 0JH, United Kingdom. FAX: 44 0161 276 5474; Mark.Wareing{at}manchester.ac.uk






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Copyright © 2006 by the Society for the Study of Reproduction.