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Platelet function in hyperbetalipoproteinemia.

R W Colman

    Thrombosis and Haemostasis
    |April 30, 1978
    PubMed
    Summary
    This summary is machine-generated.

    Familial hyperbetalipoproteinemia increases atherosclerosis risk. High cholesterol in platelets causes dysfunction, but drugs like clofibrate can normalize platelet sensitivity.

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    Area of Science:

    • Cardiovascular Biology
    • Lipid Metabolism
    • Platelet Physiology

    Background:

    • Familial hyperbetalipoproteinemia is linked to premature atherosclerosis and thrombosis.
    • Platelet function abnormalities, including aggregation and nucleotide release, are observed in this condition.

    Purpose of the Study:

    • To investigate the role of altered platelet membrane cholesterol in familial hyperbetalipoproteinemia.
    • To evaluate the effects of cholesterol enrichment and specific drugs on platelet function.

    Main Methods:

    • In vitro platelet aggregation and nucleotide release assays.
    • Measurement of cholesterol-to-phospholipid ratio in platelet membranes and lipoproteins.
    • In vitro and in vivo administration of clofibrate and halofenate.

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  • Assessment of adenylate cyclase activity and platelet membrane microviscosity.

    • Main Results:

    • Increased platelet membrane cholesterol-to-phospholipid ratio correlates with platelet hypersensitivity to aggregating agents.
    • Clofibrate and halofenate partially reverse in vitro platelet abnormalities.
    • Cholesterol enrichment increases basal adenylate cyclase but impairs prostaglandin E1 responsiveness.
    • Increased membrane microviscosity accompanies functional alterations.

    Conclusions:

    • Elevated platelet membrane cholesterol contributes to platelet hyper-reactivity in familial hyperbetalipoproteinemia.
    • Drugs affecting lipid metabolism may modulate platelet function.
    • Platelet membrane physical properties influence enzyme and receptor activity.