Hypercapnia stimulates prostaglandin E(2) but not prostaglandin I(2) release in 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 present study we address the hypothesis that microvascular endothelial cells of human fetal cerebrum increase the synthesis of dilator prostanoids in response 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 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 E(2) and 6-keto-prostaglandin F(1alpha) (the stable metabolite of prostaglandin I(2)) were measured by radioimmunoassay. Endothelial cells cultured from human fetal brain microvessels express PGE(2) and 6-keto-PGF(1alpha) in different degrees. Hypercapnic stimulus induced a significant increase of PGE(2), while expression of 6-keto-PGF(1alpha) was not augmented by the same stimulus. PGE(2) of endothelial origin, therefore, could be a factor in the mediation of the hypercapnia-induced vasodilation in human fetuses.