Prostacyclin Deficiency and Reduced Fetoplacental Blood Flow in Pregnancy-Induced Hypertension and Preeclampsia

Background: Low endothelial generation of prostacyclin (PGI 2 ) is a typical feature of pregnancy-induced hypertensive disorders. The aim of the current study was to establish whether changes in PGI 2 are accompanied by alterations in fetoplacental blood flow and to test the hypothesis that PGI 2 deficiency contributes to reduced fetoplacental perfusion in pregnancy-induced hypertension (PIH) and preeclampsia. Methods: The study included 11 women with normal pregnancies, 12 with PIH/preeclampsia, and 7 with otherwise complicated pregnancies. Fetoplacental blood flow was assessed both by umbilical artery Doppler sonography measuring the resistance index (RI) and by means of neonatal birth weight. PGI 2 formation was measured in umbilical arteries prepared immediately after birth. PGI 2 , RI and birth weight were correlated with and without correction for gestational age. Furthermore, data from patients with PIH/preeclampsia were compared with normal pregnancies as controls. Results: A significant inverse correlation was found between umbilical PGI 2 formation and umbilical RI and between birth weight and RI, whereas PGI 2 and birht weight were directly related. Patients with PIH/preeclampsia showed reduced PGI 2 formation, markedly increased gestational age-corrected RI and significantly reduced percentile birth weight. Conclusions: These results provide evidence showing that PGI 2 is a relevant mediator of fetoplacental blood flow and suggest an important role of PGI 2 deficiency in PIH/preeclampsia.