An assessment of arachidonic acid metabolism in the platelet of the neonate was performed. The uptake of [14C]arachidonic acid into platelets of both the neonate and the adult were similar. Neonatal platelets, however, released a significantly greater amount (P < .001) of prelabeled arachidonic acid (24.7% ± 2.8%) in response to the physiologic agent thrombin when compared with platelets from adult control subjects (14.6% ± 0.8%). When the activities of the lipoxygenase (12-L-hydroxy-5,8,10,14-eicosatetraenoic acid) and cyclooxygenase pathways (12-L-hydroxy-5,8,10-heptadecatrienoic acid and thromboxane B2) were evaluated following incubation of platelets with [14C]arachidonic acid, significant differences were observed between adult and neonatal platelets. Platelets from the neonate produced less (P < .01) thromboxane B2 (11.1% ± 1.7%) when compared with platelets from adult control subjects (19% ± 1.7%). In contrast, the lipoxygenase product 12-L-hydroxy-5,8,l0,14-eicostatetraenoic acid was increased (P < .005) in the platelet from the neonate (41.5% ± 2%), when compared with the adult (31.2% ± 2.1%). The observation that the availability of substrate arachidonic acid is increased in the platelet of the neonate may have general implications in neonatal pathophysiologic processes.
Arachidonic acid metabolism and pathophysiologic aspects of subarachnoid hemorrhage in rats.
