Reduced Production Of 6-Ket0-PGF1α By Umbilical Artery In Pre-Eclampsia

Abstract

Decreased production of PGI2 activity by fetal and maternal vessels and low values of PGI2 activity in amniotic fluid have recently been observed in patients with severe pre-eclampsia. In this study we measured the production of 6-keto-PGF1α by the umbilical artery and placental veins in 5 cases of severe pre-eclampsia (diastolic blood pressure > 100 mmHg) and 5 normal pregnancies. No mother had ingested aspirin for at least a week before delivery. Vascular specimens were obtained immediately after expulsion of the placenta, immersed in tris buffer 0.05 M, pH 7.4 and cut into fine rings. The production of 6 keto-PGF1α , was studied within 2 hours. Vascular fragments were incubated on a gentle rocker platform at 22°C in 2.5 ml of the following media : a) tris buffer ; b) tris buffer containing sodium arachidonate (AA) 5 pM. 100 pi subsamples were removed from the incubation dishes at 0, 4, 8, 12, 16 and 24 minutes. The 6-keto-PGF1α level in each of the subsamples was measured by radioimmunoassay. The mean values obtained, expressed as pg.mgcr-1± SEM.A significant reduction in the production of 6-keto-PGF1α by umbilical artery incubated in tris buffer (p<0.01) and tris buffer containing sodium arachidonate 5 pM (p< 0.025) was observed in the cases of severe pre-eclampsia. In contrast, no significant decrease in the production of 6-keto-PGF1α by placental veins was obtained. Considering that fetal umbilical arteries generate much greater PGI2 activity than vessels from normal adults, a central role for this substance in the regulation of fetal circulation has been postulated. The marked reduction in the production of PGI2 could seriously affect fetal outcome in severe pre-eclampsia.