Arachidonic acid metabolites and haemodynamics of the neonate

The role of eicosanoids, arachidonic acid (AA) metabolites, in blood pressure regulation under physiological and pathological conditions during the perinatal period is still under investigation. This review focuses on the synthesis and catabolism of some vasoactive AA metabolites by fetal, neonatal and placental cells, and on the vascular responses of the fetus and neonate to prostanoids and to the inhibitors of their synthesis. Vasodilator prostaglandins, PGE2 and prostacyclin (PGI2), increase steadily during pregnancy, while thromboxane A2 (TXA2), a potent vasoconstrictor, remains low during pregnancy, increasing only shortly before delivery. TXA2 participates in the closure of umbilical vessels and ductus arteriosus. In pregnancy-induced hypertension, increase in the synthesis of TXA2 occurs early during pregnancy. Decrease in the catabolism of AA precedes the onset of hypertension in the developing spontaneously hypertensive rat. In newborn piglets, platelet-activating factor, vasoconstrictor porstaglandins and leukotriene D4 have a marked constrictor effect on the pulmonary circulation and induce pulmonary hypertension, without affecting the systemic blood pressure. Although the role of AA metabolites in the regulation of haemodynamics during the perinatal period is not fully understood, it is apparent that several eicosanoids modulate the action of hormones and vasoactive agents.