Hypercapnia stimulates prostaglandin E-2 but not prostaglandin I-2 releasein endothelial cells cultured from microvessels of human fetal brain

Hypercapnia-induced cerebral vasodilation involves prostanoids, in newborns . The source of these prostanoids, however, is not yet determined. In the p resent study we address the hypothesis that microvascular endothelial cells of human fetal cerebrum increase the synthesis of dilator prostanoids in r esponse to high pCO(2-) Cells were isolated from a 22-week-old human fetus. Indication of induced abortion was 46 XY-t(3,10) 3q-25 chromosome abnormal ity. Normocapnia or hypercapnia was performed during normoxic and normother mic conditions in the medium of the cell culture. After normocapnic or hype rcapnic stimuli, the amounts of released prostaglandin E-2 and 6-keto-prost aglandin F-1 alpha (the stable metabolite of prostaglandin I-2) were measur ed by radioimmunoassay, Endothelial cells cultured from human fetal brain m icrovessels express PGE, and 6-keto-PGF(1 alpha) in different degrees. Hype rcapnic stimulus induced a significant increase of PGE(2), while expression of 6-keto-PGF(1 alpha) was not augmented by the same stimulus. PGE(2) of e ndothelial origin, therefore, could be a factor in the mediation of the hyp ercapnia-induced vasodilation in human fetuses. (C) 2001 Elsevier Science I nc.