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, adrenalin were found to be augmented in maternal blood but suppressed in the umbilical cord blood.
Plasma β-thromboglobulin level is higher in maternal and umbilical cord blood, compared with control. Plasma 6-keto-PGF1α and TxB2 values were significantly higher in umbilical cord blood than in maternal blood (p<0.05). Plasma cyclic AMP in the umbilical cord blood was significantly (p<0.001) higher than in maternal blood, but PDE activity showed no difference between mother and fetus.
A much larger amount of PGI2-like substance was released from the umbilical cord artery and vein than from the intraplacental vein and chorionic tissue. But release of that was decreased from the umbilical cord artery (4.4±2.7nmoles/mg tissue/hour) and vein (2.9±2.1) of pre-eclampsia complicated by IUGR.
These results indicate that various factors, such as PGI2, TxA2 and cyclic nucleotides, may co-exsist in high levels in fetus and the balance is needed for the maintenance of physical interaction between platelet and vascular endothelium in the fetal blood vessels.
Especially PGI2 may play an important role in this balance and in the regulation of fetoplacental circulation.