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A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Newborn platelet dysfunction: a storage pool and release defect

D G Corby, T F Zuck

    Thrombosis and Haemostasis
    |August 31, 1976
    PubMed

    Insights

    Newborn platelets show reduced aggregation and nucleotide release in response to certain stimuli, indicating potential platelet dysfunction. This may stem from decreased sensitivity and lower metabolic adenosine triphosphate (ATP) levels in infant platelets.

    Area of Science:

    • Hematology
    • Neonatal Physiology
    • Platelet Biology

    Background:

    • Platelets play a crucial role in hemostasis and thrombosis.
    • Neonatal hemostasis may differ from adult hemostasis due to developmental factors.
    • Adenine nucleotide metabolism and release are critical for platelet function.

    Purpose of the Study:

    • To evaluate platelet aggregation, adenine nucleotide release, and content in newborn infants compared to their mothers.
    • To investigate potential differences in platelet responsiveness to various agonists between neonates and adults.
    • To explore the underlying mechanisms of potential platelet dysfunction in newborns.

    Main Methods:

    • Preparation of platelet-rich plasma (PRP) from paired maternal and cord blood samples.
    • Assessment of platelet aggregation in response to adenosine diphosphate (ADP), collagen, and thrombin.
    • Measurement of adenine nucleotide release and content (ATP, ADP) in stimulated platelets.

    Main Results:

    • Newborn platelets exhibited normal aggregation to high-dose ADP, strong collagen, and thrombin.
    • Significantly reduced aggregation and impaired nucleotide release were observed in response to low-dose ADP, weak collagen, and epinephrine in newborn platelets.
    • Newborn platelets had lower ATP and ADP content compared to maternal platelets, with normal specific activity.

    Conclusions:

    • Platelet dysfunction in newborns may be characterized by decreased sensitivity to external stimuli, particularly weak agonists.
    • Impaired ADP release in neonatal platelets is likely linked to reduced responsiveness.
    • A potential lack of metabolic ATP is postulated as the cause of this platelet dysfunction in newborns.

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