The Neonatal Platelet: Evaluation of Platelet Malonyl Dialdehyde Formation as an Indicator of Prostaglandin Synthesis

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Abstract
Summary. It is recognized that neonates exhibit a transient thrombocytopathy. Whether the cause of the platelet abnormality is due to a storage pool defect, or an‘aspirin‐like’abnormality with inhibition of platelet prostaglandin synthesis is unclear. In an attempt to assess neonatal platelet prostaglandin synthesis, platelet rich plasma (PRP) from 10 normal control maternal–neonatal pairs was obtained contemporaneously with PRP from donors who had ingested 600 mg aspirin within 12‐18 h prior to study. When platelet malonyl dialdehyde production in the presence of the sulphydryl inhibitor N‐ethyl maleimide (NEM), or thrombin, was measured as an indicator of platelet prostaglandin synthesis, a significant decrease was observed in neonatal platelets (2.46 ± 0.61 and 0.90 ± 0.19 nmol/109 platelets respectively) when compared to those of the paired maternal or adult controls (3. 23 ±0.31 and 1.30 ± 0.17 nmol/109 platelets). As expected, a marked decrease in platelet malonyl dialdehyde production in response to NEM or thrombin was also seen in the platelets from the donors who had ingested aspirin (0.25±0.14 and 0.10 ± 0.09 nmol/109 platelets). When compared to the normal maternal control PRP both the neonatal and aspirin donor PRPs demonstrated abnormalities in second phase platelet aggregation in response to ADP and epinephrine, and an abnormal response to collagen. However, mutual correction and secondary irreversible aggregation was obtained when both these abnormal PRPs were mixed in varying proportions. No mutually corrective effect was seen using neonatal PRP obtained from infants where maternal documentation of aspirin ingestion was present within 48 h prior to delivery, or when normal neonatal PRP was preincu‐bated with aspirin in vitro prior to mixing with PRP from donors who had recently ingested aspirin. These findings provide evidence that the neonatal platelet dysfunction cannot be attributed to an abnormality in prostaglandin synthesis or an‘aspirin‐like’defect. Although platelet malonyl dialdehyde formation in response to NEM and thrombin was decreased when compared to the adult the amount synthesized by the neonatal platelet in response to external stimuli appears to be