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Related Experiment Videos

Released adenosine diphosphate stabilizes thrombin-induced human platelet aggregates.

M Cattaneo1, M T Canciani, A Lecchi

  • 1A.Bianchi Bonomi Hemophilia and Thrombosis Center, Maggiore Hospital, Milano, Italy.

Blood
|March 1, 1990
PubMed
Summary

Platelet aggregation is stabilized by released adenosine diphosphate (ADP). Delta-storage pool deficiency (delta-SPD) platelets, lacking ADP, are easily deaggregated, highlighting ADP's crucial role in platelet aggregate stability.

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Area of Science:

  • Hematology
  • Biochemistry
  • Platelet Physiology

Background:

  • Normal platelets aggregate and release nucleotides upon thrombin stimulation.
  • Thrombin-induced platelet aggregates are resistant to deaggregation by hirudin, chymotrypsin, and prostaglandin E1 (PGE1).
  • Platelets from patients with delta-storage pool deficiency (delta-SPD) lack releasable nucleotides.

Purpose of the Study:

  • To investigate the role of released adenosine diphosphate (ADP) in the stability of thrombin-induced platelet aggregates.
  • To determine if the lack of releasable nucleotides in delta-SPD platelets affects aggregate deaggregation.
  • To elucidate the mechanism by which ADP stabilizes platelet aggregates against deaggregation.

Main Methods:

  • Comparing the deaggregation of normal and delta-SPD platelet aggregates using a combination of inhibitors (hirudin, chymotrypsin, PGE1).

Related Experiment Videos

  • Assessing the effect of exogenous ADP and serotonin on the deaggregation of delta-SPD platelet aggregates.
  • Examining platelet aggregates from a patient with impaired ADP sensitivity (V.R.) and the impact of ADP.
  • Utilizing apyrase or creatine phosphate/creatine phosphokinase (CP/CPK) to inhibit ADP release and evaluating their effect on platelet deaggregation.

    • Main Results:

    • Thrombin-induced aggregates of delta-SPD platelets are readily deaggregated by the inhibitor combination, unlike normal platelets.
    • Exogenous ADP, but not serotonin, abolishes the deaggregation of delta-SPD platelet aggregates, indicating ADP's stabilizing role.
    • Platelet aggregates from a patient with ADP sensitivity impairment (V.R.) are also easily deaggregated, and ADP does not stabilize them.
    • Apyrase or CP/CPK treatment facilitates the deaggregation of normal platelets but does not alter the response of delta-SPD or V.R. platelets.

    Conclusions:

    • Released ADP plays a critical role in stabilizing thrombin-induced platelet aggregates, preventing their deaggregation by hirudin, chymotrypsin, and PGE1.
    • The lack of released ADP in delta-storage pool deficiency (delta-SPD) explains the enhanced deaggregation of these platelets.
    • The stabilizing effect of ADP is specific and not primarily mediated by increased fibrinogen binding sites, as epinephrine also increases binding but does not stabilize aggregates.