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Kinins and thrombolysis

J Swies1, S Chłopicki, R J Gryglewski

  • 1Department of Pharmacology, University School of Medicine, Kraków, Poland.

Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society
|June 1, 1993
PubMed
Summary

Kallikrein and captopril demonstrate thrombolytic effects in cats, dissipating blood clots. This action is linked to prostacyclin release, highlighting a potential therapeutic pathway for thrombosis.

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Area of Science:

  • Pharmacology
  • Cardiovascular Research
  • Biochemistry

Background:

  • Extracorporeal circulation models are used to study cardiovascular interventions.
  • Understanding the mechanisms of blood clot dissolution (thrombolysis) is crucial for treating thrombotic diseases.

Purpose of the Study:

  • To investigate the thrombolytic properties of kallikrein and captopril in a feline extracorporeal circulation model.
  • To elucidate the biochemical pathways involved in kallikrein-induced thrombolysis.

Main Methods:

  • Assaying arterial blood pressure and thrombolysis in cats undergoing extracorporeal circulation.
  • Administering kallikrein, captopril, and aprotinin to assess their effects on preformed blood clots.
  • Incubating thrombolytic agents with blood to identify unstable principles and their decomposition kinetics.
  • Investigating the role of aspirin in inhibiting the generation of the thrombolytic principle.

Main Results:

  • Kallikrein and captopril exhibited hypotensive and thrombolytic properties, dissolving blood clots on collagen strips.
  • A lower dose of captopril potentiated kallikrein's thrombolytic effect, while aprotinin inhibited it.
  • Kallikrein-induced thrombolysis involved an unstable factor, decomposed by blood within 15 minutes at 37°C.
  • Aspirin pretreatment inhibited the generation of this thrombolytic principle.

Conclusions:

  • The findings suggest that kallikrein-induced thrombolysis is mediated by prostacyclin, released by kinins.
  • Prostacyclin's platelet-suppressant and fibrinolytic activities contribute to thrombolysis.
  • This study identifies a potential therapeutic mechanism involving kinin-prostacyclin interaction for managing thrombosis.

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