Evaluation of Cyclo-Oxygenase Pathway in Platelets of the Newborn

A possible deficiency of cyclo-oxygenase in platelets of the newborn infant has been considered as an explanation for their impaired aggregation to stimuli which function by promoting the release of ADP. (Corby and Zuck, Thrombos. and Haemostas., USA 36:201–207, 1976). Cyclo-oxygenase activity was evaluated in washed platelets from paired mother and cord blood samples by monitoring the incorporation of radioactivity into metabolites during incubation with (1-¹⁴C) arachidonic acid. Platelets from both the mothers and newborns showed normal aggregation to arachidonic acid. Thin layer radiochromatograms of methylated incubation products were essentially identical. Three main peaks of radioactivity, which corresponded to identified arachidonic acid metabolites, were noted (Malmsten et al. Proc. Natl. Acad. Sei., USA, 72:1446–1450, 1975). Platelets from mothers and newborns incorporated similar amounts of radioactivity into 8-(1-hydroxy-3-oxopropy1)-9,12L-dihydroxy-5-10-heptadecadienoic acid (PHD) and 12L-hydroxy-5,8,10-heptadecatrienoic acid (HHT). Since these two compounds are derived from the endoperoxide prostaglandin G₂(PGG₂), which is believed to initiate the release reaction, the pathway leading from arachidonic acid to PGG₂ is probably fully developed in platelets of the newborn infant. It may be speculated that the lack of response by these platelets to external stimuli is related to either the availability or the formation of metabolically available arachidonic acid.

 

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