Abstract
Neonates manifest more hemorrhagic tendencies when exposed to either acetylsalicyclic acid (ASA) or indomethacin in comparison to adults. We therefore assessed the susceptibility of neonatal and adult platelets to the effects of these cyclooxygenase inhibitors in vitro. Baseline thromboxane B2 production in response to thrombin was similar in platelets from the adult and neonate. Following exposure to varying concentrations (0.5–100 μM) of either ASA or indomethacin, platelet thromboxane B2 was inhibited to a similar extent in both adult and neonatal platelets. Our study demonstrates that the enhanced tendency to bleeding observed in the neonate following exposure to ASA or indomethacin is not due to an enhanced susceptibility of the neonatal platelet enzyme to the effects of cyclooxygenase inhibition.