SummaryIn this study, we have investigated the possible role of the proaggregatory arachidonic acid (AA) metabolite thromboxane, in the impaired function of neonatal platelets. In platelet-rich plasma thromboxane production (measured by radioimmunoassay of thromboxane B2) was not different between neonates and adults when stimulated by thrombin (at 0.1 or 1.0 U/ml) or collagen (70μg/ml) although neonatal platelets produced decreased thromboxane (TBX2) postepinephrine stimulation. In response to 1 U/ml thrombin, adult and neonatal platelet-rich plasmas produced mean values of 3.41 ± 0.35 (SEM) and 3.11 ± 0.49 pmol of TXB2/106platelets, respectively. Production of TXB2in response to 0.1 U/ml thrombin was not dissimilar between neonates (1.01 ± 0.46 pmol) and adults (1.04 ± 0.38 pmol). When collagen was used as the aggregating agent, TXB2/production was also not significantly different with values of 2.44 ± 0.48 and 1.90 ± 0.46 pmol/106platelets produced by adult and neonatal platelet-rich plasma, respectively. In response to 200μM epinephrine, adult platelets produced 1.03 ± 0.39 pmol TXB2/106platelets while neonatal platelet TXB2production was significantly decreased (0.15 ± 0.04;P<0.05). Thromboxane production in response to AA, however, was markedly elevated in neonatal platelet-rich plasma. When 200 and 400μM concentrations of AA were used as the aggregating stimuli, neonatal platelet rich plasma produced 3.17 ± 0.77 and 8.0 ± 1.47 pmol TXB2/106platelets, respectively. These values were significantly elevatedP<0.02 and <0.005) when compared to mean values of 0.41 ± 0.10 and 3.32 ± 0.15 pmol in adult platelet-rich plasma. This elevated thromboxane production was not, however, inherent in neonatal platelets since when washed platelets were studied, results were reversed. Adult platelets produced more thromboxane at all doses of AA evaluated. These results suggest that the elevated response to exogenous AA observed in neonatal platelet-rich plasma results from as yet undetermined plasma factors. The reported deficiencies in platelet function in the newborn clearly do not result from deficient thromboxane production poststimulation with the physiologic aggregating agents collagen and thrombin. Moreover, our study introduces a new and possibly important difference between adult and neonatal plasma, namely, the differential response to exogenous arachidonic acid.