Effects of prostacyclin on fetal platelet function.

Abstract

Prostacyclin (PGI2), the major active metabolite of arachidonic acid in the vascular endothelium, is characterized by antiaggregatory and vasodilator properties. In this report the significance of PGI2 on fetal platelets was studied. Platelet aggregation induced by ADP, collagen, and adrenaline was found to be augmented in maternal blood but suppressed in umbilical cord blood. The plasma beta-thromboglobulin levels were higher in maternal and umbilical cord blood compared with that of a control group. Plasma 6-keto-PGF1 alpha, TxB2, cyclic AMP, and cyclic GMP values were significantly higher in umbilical cord blood than in maternal blood. A much larger amount of PGI2-like substance was released from the umbilical vessels than from the placental vascular tissues. The generation of this substance was reduced in the umbilical vessels in patients with severe pre-eclampsia associated with intrauterine fetal growth retardation. These results indicate that various factors, such as PGI2, TxA2, and cyclic nucleotides, may co-exist at high levels in the fetus. A balance is needed to maintain physical interaction between platelets and the vascular wall in the fetal blood vessels. Especially PGI2 may play an important role in this balance and in the regulation of the placental-fetal circulation.