Platelet-dependent thrombin generation after in vitro fibrinolytic treatment

Fibrinolytic therapy is associated with frequent rethrombosis. There is evidence of both increased coagulation and platelet activation. Platelet-rich plasma (PRP) or washed platelets were incubated with the fibrinolytic agents urokinase, recombinant tissue-type plasminogen activator (rt-PA), or plas...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1992-05, Vol.85 (5), p.1706-1712
Main Authors: ARONSON, D. L, PING CHANG, KESSLER, C. M
Format: Article
Language:English
Subjects:
Biological and medical sciences
Blood Platelets - physiology
Blood. Blood coagulation. Reticuloendothelial system
Fibrinolysin - pharmacology
Fibrinolytic Agents - pharmacology
Humans
Medical sciences
Pharmacology. Drug treatments
Plasminogen Activators - pharmacology
Recombinant Proteins
Thrombin - analysis
Thrombin - biosynthesis
Tissue Plasminogen Activator - pharmacology
Urokinase-Type Plasminogen Activator - pharmacology
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Summary:Fibrinolytic therapy is associated with frequent rethrombosis. There is evidence of both increased coagulation and platelet activation. Platelet-rich plasma (PRP) or washed platelets were incubated with the fibrinolytic agents urokinase, recombinant tissue-type plasminogen activator (rt-PA), or plasmin at concentrations consistent with those in the plasma of patients treated for myocardial infarction. All of the fibrinolytic agents induced a more rapid generation of thrombin and decreased the clotting times of non-contact-activated PRP than in untreated PRP. This effect was not blocked by the inclusion of thrombin inhibitors during the fibrinolytic treatment. Washed platelets derived from rt-PA-treated PRP induced more rapid thrombin generation when resuspended in untreated plasma or treated plasma. Washed platelets were treated with plasmin, rt-PA, and urokinase and added to platelet-poor plasma. Platelets treated with either plasmin or rt-PA increased the ability of washed platelets to support thrombin generation, but urokinase was without significant effect. These results indicate not only that plasmin can cause increased platelet support of prothrombin activation but also that rt-PA in the absence of plasminogen can have a direct effect on the platelet, which increases thrombin generation.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.85.5.1706