Altered Regulation Of Prostacyclin (PGI2) Activity In Severe Pre-Eclampsia

It has been suggested that prostaglandins of the E series play a crucial role in regulation of fetal vascular tone. The discovery of PGI2 has opened new perspectives for understanding the circulatory physiology of normal pregnancy and the vascular abnormalities of pre-eclampsia. We have bioassayed PGl2 platelet antiaggregatory activity and confirmed it by RIA of 6-Keto-PGF1α and thin-layer radiochranatograpty in human umbilical and piacental vessels. Fetal umbilical arteries obtained at the end of 9 uncomplicated pregnancies generated significantly more PGI2 (191 ± 29 ng/mg tissue) than vessels from control non pregnant adults (43 ± 12 ng/ mg) (p < 0.01). Placental veins generated PGI2 similarly to control veins (33 ± 7 and 37 ± 8 ng/mg respectively) . This could contribute to maintaining the lew peripheral vascular resistance of the fetal circulation with very high cardiac output. Umbilical arteries from 5 vramen with severe preeclampsia generated significantly less PGI2 (65 ± 12 ng/mg tissue) than the corresponding vessels from women with normal pregnancy (p < O.Ol). Similarly placental veins frem preeclampsia patients generated less PGI2 (11 ± 2) than normal pregnancy veins (p<0.01). We propose that in severe pre-eclampsia,placental ischemia and fetal distress could be triggered by deficiency of the adaptive mechanism which maintains high vascular levels of PGI2 in normal pregnancy. The abnormally high PGI2 stirnulating activity in plasma frem patients with severe pre-eclampsia in comparison with plasma from women with normal pregnancy supports the contention that regulation of PGI2 synthesis is deranged in pre-eclampsia.