THROMBOXANE AND PROSTACYCLIN IN MATERNAL AND FETAL CIRCULATION IN PREECLAMPSIA

Objectives: A major pathophysiologic change of pre-eclampsia has been attributed to the overproduction of thromboxane A(2) (TXA(2)) mainly f rom activated platelets. On the other hand, increased biosynthesis of TXA(2) has also been reported from preeclamptic placentas. The systemi c role of these different sources of TXA(2) has not been clarified. Th e purpose of this study is to define the changes of TXA(2) and the ant agonizing prostacyclin (PC) in maternal and fetal circulations. Method s: The stable metabolites of TXA(2) and PC [Thromborrine B-2 (TXB2) an d 6-keto-prostaglandin F(1)alpha (6-keto-PGF(1)alpha), respectively] i n 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 +/- 2 63 vs. 12.5 +/- 3.9 ng/ml, P < 0.05) levels than the maternal blood. I n the preeclamptic state, a marked increase of TXB2 was noted in both maternal and cord blood, reaching levels which were significantly high er than during normal pregnancy (2995 +/- 1103 vs. 267 +/- 128 ng/ml i n 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 th e diastolic blood pressure of preeclamptic patients before and after d elivery. Conclusion: The results suggest an abundant source of eicosan oids in the feto-placental circulation, which does not readily cross t he placental barrier. In pregnancy complicated with pre-eclampsia, thr omboxane level of both fetal and maternal circulations are markedly in creased, which may be responsible for the pathophysiologic changes. Th e 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 a nd Obstetrics.