Fibrinolysis and thrombosis.
In conclusion, venous and arterial thrombi contain significant amounts of fibrin. There is evidence that defective fibrinolytic mechanisms may participate in their genesis or persistence in the body. Some evidence suggests that defective fibrinolysis may presage and predict both arterial and venous thrombi; this is stronger evidence of a causal link with thrombosis. Thrombi protect themselves from lysis by incorporating inhibitors (plasminogen activator inhibitor-1 and alpha 2-antiplasmin) in their structure. Fibrinolytic mechanisms may play a role in the genesis or development of atherosclerotic lesions, in addition to thrombosis. Thrombolytic agents lyse both arterial and venous thrombi when administered shortly after their development. If it proves possible in future to enhance natural fibrinolytic mechanisms and to sustain this enhancement by pharmacological or other means, the interesting prospect of harnessing the fibrinolytic system to prevent thrombus formation, as well as to treat it, will arise.
Department of Molecular & Cell Biology, University of Aberdeen, Marischal College, UK.
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Booth
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Bennett
D000818:Animals; D000933:Antifibrinolytic Agents / Q000378:metabolism; D001158:Arteries; D001161:Arteriosclerosis / Q000097:blood; D001779:Blood Coagulation Factors / Q000502:physiology; D005342:Fibrinolysis / Q000502:physiology; D020022:Genetic Predisposition to Disease; D006801:Humans; D017395:Plasminogen Activator Inhibitor 1 / Q000502:physiology; D013924:Thrombophlebitis / Q000097:blood; D013927:Thrombosis / Q000097:blood*
D000933:Antifibrinolytic Agents; D001779:Blood Coagulation Factors; D017395:Plasminogen Activator Inhibitor 1