To study the production of proaggregatory thromboxane A2(TxA2) by fetal and neonatal platelets, blood specimens were collected from umbilical cords immediately after delivery at term (n = 22), from newborn infants during the first 10 days of life (n = 85), from infants between 1 and 3 months of age (n = 14), and from healthy adults (n = 18). The blood samples were allowed to clot spontaneously at +37±C for 60 min, and the concentrations of thromboxane B2(TxB2), a stable metabolite of TxA2, in the sera were measured by radioimmunoassay and expressed as nanograms of TxB2/106platelets.Platelet TxB2generation in term infants at the age of 1 day (1.344 ± 0.253 ng/106platelets, mean ± SE, n = 9) was higher than that in cord blood (0.634 ± 0.042 ng/106platelets, n = 22), or in infants of 1–3 months of age (0.881 ± 0.099 ng/106platelets, n = 14), or in adults (0.869 ± 0.062 ng/106platelets, n = 18). Increase in TxB2generation following birth was seen already at the age of 1 h (1.076 ± 0.114 ng/106platelets, n = 9). TxB2synthesis in preterm infants (1.032 ± 0.136 ng/106platelets, n = 10) did not differ from that in term infants on the 1st day of life, and idiopathic respiratory distress syndrome had no effect on it (1.029 ± 0.079 ng/106platelets, n = 19). Severe birth asphyxia was accompanied by reduced TxB2formation (0.564 ± 0.201 ng/ 106platelets, n = 7).The mode of delivery, the birth weight, and the sex of the infants were not related to TxB2production on the 1st day of life. Neither maternal pre-eclampsia nor epidural analgesia during labor affected neonatal TXB2generation. The bleeding time also did not correlate with TxB2formation. It is suggested that a rapid, but transient stimulation in TxA2synthesis after birth may contribute to the neonatal adaptation of vascular platelet function.