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Related Experiment Videos

Aprotinin: is it prothrombotic?

M Poullis1, R C Landis, K M Taylor

  • 1National Heart and Lung Institute, Imperial College School of Medicine at Hammersmith, London, UK. mpoullis@hotmail.com

Perfusion
|September 22, 2001
PubMed
Summary
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Aprotinin (Trasylol) does not affect platelet aggregation from common agonists. However, it inhibits thrombin-induced platelet activation, suggesting a specific mechanism involving protease-activated receptors (PARs).

Area of Science:

  • Biochemistry
  • Pharmacology
  • Hematology

Background:

  • Aprotinin (Trasylol) is a controversial drug regarding its prothrombotic potential.
  • The discovery of protease-activated receptors (PARs) has provided new insights into drug mechanisms.
  • Understanding aprotinin's interaction with platelet activation pathways is crucial.

Purpose of the Study:

  • To investigate the effect of aprotinin on platelet aggregation and activation.
  • To determine if aprotinin's mechanism involves protease-activated receptors (PARs).
  • To clarify the prothrombotic controversy surrounding aprotinin.

Main Methods:

  • Assessing platelet aggregation induced by various agonists: adrenaline, adenosine diphosphate, phorbol-12-myristate-13-acetate, collagen, and a PAR 1 agonist peptide.

Related Experiment Videos

  • Evaluating thrombin-induced platelet activation using macroaggregation, microaggregation, and platelet membrane calcium flux assays.
  • Analyzing the role of proteolytic versus non-proteolytic platelet activation mechanisms.

    • Main Results:

    • Aprotinin demonstrated no significant effect on platelet aggregation induced by adrenaline, adenosine diphosphate, phorbol-12-myristate-13-acetate, collagen, or PAR 1 agonist peptide.
    • Aprotinin significantly inhibited thrombin-induced platelet activation, as evidenced by macroaggregation, microaggregation, and calcium flux.
    • The results indicate that aprotinin specifically inhibits proteolytic platelet activation pathways.

    Conclusions:

    • Aprotinin does not inhibit platelet aggregation mediated by common, non-proteolytic pathways.
    • Aprotinin selectively inhibits thrombin-induced platelet activation, likely through mechanisms involving protease-activated receptors (PARs).
    • This suggests a specific inhibitory action on proteolytic platelet activation, rather than a general prothrombotic effect.