Hypercapnia stimulates prostaglandin E2 but not prostaglandin I2 release in endothelial cells cultured from microvessels of human fetal brain

K. Kövecs, K. Komjáti, T. Marton, J. Skopál, P. Sándor, Z. Nagy

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Hypercapnia-induced cerebral vasodilation involves prostanoids, in newborns. The source of these prostanoids, however, is not yet determined. In the present study we address the hypothesis that microvascular endothelial cells of human fetal cerebrum increase the synthesis of dilator prostanoids in response to high pCO2. Cells were isolated from a 22-week-old human fetus. Indication of induced abortion was 46 XY-t(3,10) 3q-25 chromosome abnormality. Normocapnia or hypercapnia was performed during normoxic and normothermic conditions in the medium of the cell culture. After normocapnic or hypercapnic stimuli, the amounts of released prostaglandin E2 and 6-keto-prostaglandin F (the stable metabolite of prostaglandin I2) were measured by radioimmunoassay. Endothelial cells cultured from human fetal brain microvessels express PGE2 and 6-keto-PGF in different degrees. Hypercapnic stimulus induced a significant increase of PGE2, while expression of 6-keto-PGF was not augmented by the same stimulus. PGE2 of endothelial origin, therefore, could be a factor in the mediation of the hypercapnia-induced vasodilation in human fetuses.

Original languageEnglish
Pages (from-to)387-390
Number of pages4
JournalBrain Research Bulletin
Issue number4
Publication statusPublished - Mar 1 2001



  • Fetal brain endothelium
  • Hypercapnia
  • Prostaglandin E
  • Prostaglandin I

ASJC Scopus subject areas

  • Neuroscience(all)

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