Thromb Haemost 1976; 36(01): 200-207
DOI: 10.1055/s-0038-1648025
Original Article
Schattauer GmbH

Newborn Platelet Dysfunction: a Storage Pool and Release Defect[*]

Donald G. Corby
**  Clinical Investigation Service, San Francisco, Calif.
,
Thomas F. Zuck
***  Fitzsimons Army Medical Center, Denver, Co., and Letterman Army Institute of Research, San Francisco, Calif.
› Author Affiliations
Further Information

Publication History

Received 18 August 1975

Accepted 20 January 1976

Publication Date:
03 July 2018 (online)

Summary

Per cent aggregation, release and content of adenine nucleotides, and specific radioactivity were evaluated in citrated platelet-rich plasma (PRP) prepared from paired samples of maternal and cord blood. Platelets of newborn infants aggregated normally in response to high dose ADP (20 μM), strong collagen suspensions, and thrombin; however, when compared with PRP from the mothers or from normal adults, per cent aggregation in response to lower concentrations of ADP (2 μM), weak collagen, and part particularly epinephrine was markedly reduced. Nucleotide release after stimulation of the newborns’ PRP with the latter two inducers was also impaired. ATP and ADP content of the newborns’ platelets was also significantly less than that of their mothers or of normal adults, but specific activity was normal. The data suggest that the impairment of ADP release in the platelets of newborn infants is due to decreased sensitivity to external stimuli. Since metabolic ATP is necessary for the platelet release reaction, it is postulated that the platelet dysfunction results from a lack of metabolic ATP.

* Presented in part at the 44th Annual Meeting of the Society for Pediatric Research, Washington, D. C, May, 1974.

* The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.