Neonatal platelet function: a membrane-related phenomenon?

Synthesis of prostaglandin endoperoxides was evaluated in paired maternal and cord blood samples. Platelets from mothers and neonates aggregated normally in response to arachidonic acid (AA). Cyclooxygenase activity was evaluated by monitoring the incorporation of radioactivity into prostaglandin endoperoxide metabolites after incubation with 1-14C-AA. Thin layer radiochromatograms of methylated incubation products revealed three main peaks corresponding to 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid, 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT), and 8-(1-hydroxy-3-oxoproply)-9,12-L-dihydroxy-5,10-heptadecadienoic acid (TXB2). Maternal and neonatal platelets incorporated similar amounts of radioactivity into HHT and TXB2. Radioimmunoassay for TXB2 in thrombin-clotted PRP revealed no significant differences between maternal and neonatal platelets. Since these metabolites are derived from cyclic endoperoxides formed by the action of cyclooxygenase on AA, we conclude that prostaglandin endoperoxide synthesis is fully developed in neonatal platelets. Mutual correction of collagen-induced platelet aggregation and ADP release was observed when equal volumes of neonatal and aspirin-treated adult platelet-rich plasma were mixed. Therefore, since neonatal platelets contain normal amounts of storage pool nucleotides, we also conclude that the defective secondary aggregation and release seen in neonatal platelets is caused by a failure in the release of AA from membrane phospholipids upon stimulation with collagen or epinephrine.