Role of Plasminogen Activator Inhibitor-1 in Promoting Fibrin Deposition in Rabbits Infused with Ancrod or Thrombin
Abstract
The role of defective, fibrinolysis caused by elevated activity of plasminogen activator inhibitor-1 (PAI-1) in promoting fibrin deposition in vivo has not been well established. The present study compared the efficacy of thrombin or ancrod, a venom-derived enzyme that clots fibrinogen, to induce fibrin formation in rabbits with elevated PAI-1 levels. One set of male New Zealand rabbits received intravenous endotoxin to increase endogenous PAI-1 activity followed by a 1 -hour infusion of ancrod or thrombin; another set of normal rabbits received intravenous human recombinant PAI-1 (rPAI-1) during an infusion of ancrod or thrombin. Thirty minutes after the end of the infusion, renal fibrin deposition was assessed by histopathology. Animals receiving endotoxin, rPAI-1 , ancrod, or thrombin alone did not develop renal thrombi.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 15, 1993
- Accession Number
- ADA275301
Entities
People
- Barbara M. Alving
- Charles Bolan
- Chitra Krishnamurti
- Curtis A. Colleton
- Thomas M. Reilly
Organizations
- Walter Reed Army Institute of Research