Increased thromboxane A2 production but normal prostacyclin by the placenta in hypertensive pregnancies.

The production of vasodilatory, antiaggregatory prostacyclin (PGI2) and vasoconstrictory, proaggregatory thromboxane A2 (TxA2) by the placenta was studied in the cases of hypertensive pregnancy complications by superfusing pieces from maternal and fetal sides of placentae of 9 pre-eclamptic, 6 hypertensive and 11 healthy women in vitro and measuring the release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2), the breakdown products of PGI2 and TxA2 respectively, from the superfusate. Both sides of the placentae from the controls produced 6-keto-PGF1 alpha (maternal side 0.5 +/- 0.1 ng/g/min dry weight of tissue, mean +/- SEM; fetal side 0.7 +/- 0.2 ng/g/min) and TxB2 (maternal side 2.5 +/- 0.4 ng/g/min; fetal side 2.7 +/- 0.5 ng/g/min) with no correlation between the two. The 6-keto-PGF1 alpha production was normal in hypertensive complications whereas the TxB2 production was increased on the fetal side of the placentae obtained from the pre-eclamptic (3.7 +/- 0.3 ng/g/min: p less than 0.05) and hypertensive women (4.1 +/- 0.4 ng/g/min; p less than 0.025). This may explain the occurrence of microthrombi and infarctions in placentae of hypertensive women.