Thrombin hypothesis of thrombus generation and vascular lesion formation

Thrombin plays a central role in vascular lesion formation. It is the principal mediator of thrombogenesis, which is interrupted when direct antithrombins (including hirudin and its synthetic peptide analogs), thrombin receptor antagonist peptides, or thrombin generation inhibitors (including active...

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Bibliographic Details
Published in:The American journal of cardiology 1995-02, Vol.75 (6), p.12B-17B
Main Authors: Harker, Laurence A., Hanson, Stephen R., Runge, Marschall S.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cardiovascular disease
Cell Division - drug effects
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Enzymes
Humans
Leukocytes
Medical research
Medical sciences
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - pathology
Receptors, Thrombin - antagonists & inhibitors
Receptors, Thrombin - physiology
Thrombin - antagonists & inhibitors
Thrombin - physiology
Thrombosis - etiology
Thrombosis - metabolism
Thrombosis - pathology
Vasculitis - etiology
Vasculitis - metabolism
Vasculitis - pathology
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Summary:Thrombin plays a central role in vascular lesion formation. It is the principal mediator of thrombogenesis, which is interrupted when direct antithrombins (including hirudin and its synthetic peptide analogs), thrombin receptor antagonist peptides, or thrombin generation inhibitors (including active-site inhibited factor VIIa, recombinant tick anticoagulant peptide, and omega-3 fatty acids) are used to block thrombin. Thrombin is also a potent growth factor, initiating smooth muscle cell proliferation at injury sites. In baboons, this reaction is 80% reduced by hirudin ( p
ISSN:0002-9149
1879-1913
DOI:10.1016/0002-9149(95)80004-C