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Related Experiment Videos

"Plasminogen steal" and clot lysis.

S R Torr1, D A Nachowiak, S Fujii

  • 1Cardiovascular Division, Washington University School of Medicine, Saint Louis, Missouri 63110.

Journal of the American College of Cardiology
|April 1, 1992
PubMed
Summary

Second-generation thrombolytic agents paradoxically impair clot lysis by depleting clot-associated plasminogen. Supplementing with plasminogen preserves it, enhancing clot lysis and recanalization.

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Area of Science:

  • Biochemistry
  • Hematology
  • Thrombosis Research

Background:

  • Second-generation thrombolytic agents offer improved recanalization over first-generation agents.
  • The mechanism by which clot-selective agents preserve clot-associated plasminogen remains unclear.

Purpose of the Study:

  • To investigate whether second-generation thrombolytic agents preserve clot-associated plasminogen.
  • To determine the effect of plasminogen levels on clot lysis mediated by recombinant tissue-type plasminogen activator (rt-PA).

Main Methods:

  • Human whole blood clots were formed and incubated with varying concentrations of rt-PA.
  • Clot-associated plasminogen levels were quantified using Western blot analysis.
  • Clot lysis was assessed in the presence and absence of supplemental plasminogen or fibrinogen degradation products.

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Main Results:

  • Suprapharmacologic concentrations of rt-PA paradoxically impaired clot lysis and depleted clot-associated plasminogen.
  • Supplementation with plasminogen conserved both plasma and clot-associated plasminogen, preventing lysis diminution.
  • Fibrinogen degradation products did not inhibit lysis and may potentiate rt-PA activity.

Conclusions:

  • Second-generation thrombolytic agents, like rt-PA, can deplete clot-associated plasminogen, leading to impaired clot lysis.
  • Maintaining adequate plasminogen levels is crucial for effective thrombolysis and clot recanalization.
  • Understanding plasminogen dynamics is key to optimizing thrombolytic therapy.