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Updated: Jul 14, 2026

Mouse Complete Stasis Model of Inferior Vena Cava Thrombosis
04:34

Mouse Complete Stasis Model of Inferior Vena Cava Thrombosis

Published on: June 15, 2011

Plasmin inhibition increases MMP-9 activity and decreases vein wall stiffness during venous thrombosis resolution

Nicholas A Dewyer1, Vikram Sood, Erin M Lynch

  • 1Jobst Vascular Surgery Laboratory, Section of Vascular Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA.

The Journal of Surgical Research
|June 19, 2007
PubMed
Abstract

Insights

Pharmacological inhibition of the plasmin system led to larger deep venous thrombosis (DVT) but reduced vein wall injury in rats. This suggests a redundant mechanism for DVT resolution involving matrix metalloproteinase-9 (MMP-9).

Area of Science:

  • Vascular Biology
  • Thrombosis Research
  • Biomedical Science

Background:

  • Deep venous thrombosis (DVT) resolution involves complex interactions between the plasmin and matrix metalloproteinase (MMP) systems.
  • Understanding these interactions is crucial for developing effective DVT treatments.
  • This study investigates the impact of inhibiting the plasmin system on DVT resolution and associated vein wall damage.

Purpose of the Study:

  • To test the hypothesis that pharmacological inhibition of the plasmin system impairs DVT resolution and exacerbates vein wall damage.
  • To elucidate the role of MMPs in the context of plasmin system inhibition during DVT resolution.

Main Methods:

  • A rat model of stasis deep venous thrombosis (DVT) was established via inferior vena cava (IVC) ligation.
  • Rats received intravenous control saline or aprotinin (AP) to inhibit the plasmin system.
  • Thrombosed IVCs were analyzed after 7 days for thrombus weight, perfusion, collagen, d-dimer, MMP-2, MMP-9, inflammatory markers, and leukocyte infiltration.

Main Results:

  • Aprotinin treatment resulted in significantly larger DVT weights (2-fold increase) compared to controls.
  • Vein wall stiffness was reduced by 50% in AP-treated rats, indicating less biomechanical injury.
  • A significant 5-fold increase in vein wall MMP-9 activity was observed in the AP group, suggesting its compensatory role in DVT resolution.

Conclusions:

  • Inhibition of the plasmin system with aprotinin leads to larger thrombi but reduced vein wall injury.
  • Increased vein wall MMP-9 activity may represent a redundant mechanism for DVT resolution.
  • These findings highlight the complex interplay of enzymatic systems in DVT resolution and suggest potential therapeutic targets.

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