Abstract
We present a peculiarity of the neonatal hemostatic system that might contribute to establish a procoagulant readiness in neonatal blood by sensitizing neonatal platelets for ADP stimulation. β2-glycoprotein-I (β2-GP-I) is a plasma constituent capable of suppressing ADP-induced platelet aggregation. We found significant lower levels of β2-GP-I in cord vs. adult plasma (120 ± 27 vs. 180 ± 37 µg/mL, P < 0.001). We demonstrate dose-dependent inhibition of ADP-induced platelet aggregation in cord whole blood (WB) in the presence of increasing amounts of β2-GP-I, evaluated by means of WB aggregometry employing the impedance method. Particularly, raising the β2-GP-I concentration in cord WB from neonatal level up to the respective adult value caused significant reduction of amplitude (from 9.5 ± 2.7 to 2.8 ± 0.9 Ω, P < 0.001) and of slope (from 5.9 ± 2.4 to 1.89 ± 0.9 Ω/min, P < 0.001), and a significant prolongation of the aggregation time (from 51.8 ± 22.9 to 110.8 ± 60.3 s, P < 0.001). In conclusion, physiological low levels of β2-GP-I in cord WB cause enhanced responsiveness of neonatal platelets to ADP stimulation. This mechanism might help to explain the clinically observed well-functioning hemostasis in neonates.
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