Role of Plasminogen Activator Inhibitor-1 in Promoting Fibrin Deposition in Rabbits Infused with Ancrod or Thrombin

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 fi...

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Bibliographic Details
Main Authors: Krishnamurti, Chitra, Bolan, Charles, Colleton, Curtis A, Reilly, Thomas M, Alving, Barbara M
Format: Report
Language:English
Subjects:
ANIMALS
Biochemistry
BLOOD COAGULATION
DEPOSITION
ENDOTOXINS
ENZYME PRECURSORS
ENZYMES
FIBRIN
FIBRINOGEN
FIBRINOLYSIS
HISTOPATHOLOGY
HUMANS
IN VIVO ANALYSIS
INFUSIONS
INHIBITORS
MALES
NEW ZEALAND
PHYSIOLOGY
RABBITS
REPRINTS
THROMBIN
VENOMS
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Summary: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. Pub. in Blood, v82, n12, p3631-3636, 15 Dec 1993.