Thromboxane and prostacyclin in maternal and fetal circulation in pre-eclampsia

Objectives: A major pathophysiologic change of pre-eclampsia has been attributed to the overproduction of thromboxane A(2) (TXA(2)) mainly from activated platelets. On the other hand, increased biosynthesis of TXA(2) has also been reported from preeclamptic placentas. The systemic role of these different sources of TXA(2) has not been clarified. The purpose of this study is to define the changes of TXA(2) and the antagonizing prostacyclin (PC) in maternal and fetal circulations. Methods: The stable metabolites of TXA(2) and PC [Thromborrine B-2 (TXB2) and 6-keto-prostaglandin F(1)alpha (6-keto-PGF(1)alpha), respectively] in the cord and maternal blood of nine patients with pre-eclampsia and nine normal parturients were measured by radioimmunoassay. Result: In normal pregnancy, the cord blood contained much higher TXB2 (1697 +/- 898 vs. 267 +/- 128 ng/ml, P < 0.01) and 6-keto-PGF(1)alpha (266 +/- 263 vs. 12.5 +/- 3.9 ng/ml, P < 0.05) levels than the maternal blood. In the preeclamptic state, a marked increase of TXB2 was noted in both maternal and cord blood, reaching levels which were significantly higher than during normal pregnancy (2995 +/- 1103 vs. 267 +/- 128 ng/ml in maternal blood, P < 0.0001, and 3197 +/- 1288 vs. 1697 +/- 898 ng/ml in cord blood, P < 0.005). A less significant increase in 6-keto-PGF(1)alpha (134 +/- 10.8 vs. 12.5 +/- 3.9 ng/ml, P < 0.05) was also noted in the maternal blood. Moreover, the level of TXB2 correlated with the diastolic blood pressure of preeclamptic patients before and after delivery. Conclusion: The results suggest an abundant source of eicosanoids in the feto-placental circulation, which does not readily cross the placental barrier. In pregnancy complicated with pre-eclampsia, thromboxane level of both fetal and maternal circulations are markedly increased, which may be responsible for the pathophysiologic changes. The lack of adverse systemic effects on the fetus highlights a placental source of TXA(2) of transient bioactivity which is rapidly hydrolyzed to non-active TXB2. (C) 1998 International Federation of Gynecology and Obstetrics.