Association of whole blood aggregation response with immunogold-labeled glycoproteins in adult and neonatal platelets

A growing body of recent data has provided specifics about the hemostatic system in infants, emphasizing differences from adults. Although platelet structure in newborns and adults appears to be quite similar, precise information about platelets in the first week of life indicates functional hyporeactiveness. This study was designed with a twofold purpose: one was to determine if aggregation results corresponded to immunogold-labeled activation markers; the second was to use immunogold labeling to determine if infant platelets circulate in an activated state. The results showed significant differences in ristocetin (P = .03) and collagen (P = .003) impedance, and whole blood aggregation lag times in infants when compared to adults. Treatment of neonatal platelets with collagen yielded decreased ATP release compared with adults. Immunogold labeling of specific activation markers CD62 (P-selectin) and CD63 (GP53) revealed that neonatal platelets were not circulating in an activated state. Significant (P = .04) anti-CD41 (GPIIb) immunogold labeling differences were observed after thrombin stimulation, with adults binding more particles. These data suggest that hyporeactivity of neonatal platelets is not due to a circulating preactivated state, but instead may be a consequence of impaired intracellular signaling that affects both aggregation and membrane activation labeling. Whether this signaling is secondary to an intrinsic neonatal alteration or a maternal (in utero) environmental effect is yet to be determined.