Prostacyclin and thromboxane during human pregnancy.
The implications of the antiaggregatory and vasodilatory prostacyclin (PGI2) and proaggregatory and vasoconstrictory thromboxane A2 (TxA2) during human pregnancy in vivo are briefly reviewed. The level of circulating PGI2 in maternal plasma, as measured by its metabolite (= 6-keto-PGF1a) levels, rises during parturition, but there is no conclusive evidence that the PGI2 production increases already during pregnancy. In pre-eclampsia, PGI2 production can decrease, at least in amniotic fluid, but it is not known whether this PGI2 deficiency is a primary or secondary change in the pre-eclamptic state. TxA2 production in the maternal blood, as measured by the plasma and serum levels of TxB2, is increased during pregnancy, but the effect of pregnancy complication on its production is not known. In amniotic fluid, however, the TxB2 levels did not differ between normal and pre-eclamptic pregnancies. Further in vivo studies are needed to prove or reject the theory that a shift in the PGI2/TxA2 balance to a TxA2 predominance could be of etiological significance in preeclampsia or other pregnancy complications.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood / Q000378:metabolism; D000653:Amniotic Fluid / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism*; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D006801:Humans; D011225:Pre-Eclampsia / Q000378:metabolism; D011247:Pregnancy; D011453:Prostaglandins / Q000378:metabolism*; D013928:Thromboxane A2 / Q000378:metabolism*; D013929:Thromboxane B2 / Q000378:metabolism; D013931:Thromboxanes / Q000378:metabolism*
D011453:Prostaglandins; D013931:Thromboxanes; D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol