Decreased prostacyclin production by placental cells in culture from pregnancies complicated by fetal growth retardation

M. Jogee, Leslie Myatt, M. G. Elder

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

Production of prostacyclin (PGI2) in vitro by human placental cells from pregnancies complicated by fetal growth retardation was significantly reduced compared with that in placental cells from normal pregnancies of either matched gestation or at term. This appeared to be due to a reduction of synthesis of PGI2 rather than to any alteration in the rate of its enzymic metabolism. Addition of oestradiol and progesterone increased PGI2 production by cells from pregnancies with fetal growth retardation in a similar manner to that by cells from first trimester pregnancies, implying that the placental cells are not irreversibly damaged by ischaemia. The decreased PGI2 production by cells of trophoblastic origin may be an aetiological factor in the thrombotic occlusion of the uteroplacental circulation which impairs fetal growth.

Original languageEnglish (US)
Pages (from-to)247-250
Number of pages4
JournalBritish Journal of Obstetrics and Gynaecology
Volume90
Issue number3
StatePublished - 1983
Externally publishedYes

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Fetal Growth Retardation
Epoprostenol
Cell Culture Techniques
Pregnancy
Placental Circulation
First Pregnancy Trimester
Fetal Development
Progesterone
Estradiol
Ischemia

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

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