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. beta2-glycoprotein-I (beta2-GP-I) is a plasma constituent capable of suppressing ADP-induced platelet aggregation. We found significant lower levels of beta2-GP-I in cord vs. adult plasma (120 +/- 27 vs. 180 +/- 37 microg/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 beta2-GP-I, evaluated by means of WB aggregometry employing the impedance method. Particularly, raising the beta2-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 Omega, P<0.001) and of slope (from 5.9 +/- 2.4 to 1.89 +/- 0.9 Omega/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 beta2-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.
journal_name
Plateletsjournal_title
Plateletsauthors
Cvirn G,Gallistl S,Koestenberger M,Kutschera J,Ferstl U,Kellner J,Jurgens G,Gries Adoi
10.1080/09537100600800529subject
Has Abstractpub_date
2007-02-01 00:00:00pages
24-8issue
1eissn
0953-7104issn
1369-1635pii
770734491journal_volume
18pub_type
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