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Related Experiment Videos

Endothelial dysfunction following thrombolysis in vitro

A d'Audiffret1, P Soloway, R Saadeh

  • 1Department of Surgery, SUNY at Buffalo, Millard Fillmore Hospital, NY 14209, USA.

European Journal of Vascular and Endovascular Surgery : the Official Journal of the European Society for Vascular Surgery
|January 23, 1999
PubMed
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Vascular graft thrombosis is poorly managed by thrombolytic therapy. Endothelial cells (ECs) retract after thrombus exposure, potentially increasing graft thrombogenicity despite enhanced thromboresistance markers.

Area of Science:

  • Vascular biology
  • Thrombosis research
  • Endothelial cell function

Background:

  • Thrombolytic therapy is a common treatment for vascular graft thrombosis.
  • Long-term patency of vascular grafts after thrombolysis is often suboptimal.

Purpose of the Study:

  • To investigate the response of endothelial cells (ECs) to thrombus exposure.
  • To characterize EC changes following thrombolysis with urokinase.

Main Methods:

  • Human ECs were incubated with whole blood thrombus for varying durations (2-24 hours).
  • Cell morphology was assessed via electron microscopy.
  • Gene expression of key proteins (endothelin-1, thrombomodulin, tissue factor, tPA, PAI) was analyzed using Northern blot.

Main Results:

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  • Endothelial cell retraction was observed at all time points.
  • Thrombomodulin expression increased significantly, suggesting enhanced thromboresistance.
  • Tissue plasminogen activator (tPA) expression decreased with prolonged thrombus exposure.
  • Plasminogen activator inhibitor (PAI) and tissue factor (TF) showed transient increases.

Conclusions:

  • Endothelial cells exposed to thrombus do not become significantly procoagulant.
  • Increased thrombomodulin suggests a thromboresistant response.
  • Endothelial cell retraction may contribute to increased graft thrombogenicity after thrombolysis.