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Liquefaction of coagulated blood by the action of plasmin on fibrin.



the dissolution of intravascular thrombi and extravascular deposits of fibrin by the enzyme fibrinolysin. Fibrinolysis is important for keeping the blood liquid and the blood vessels and glandular ducts patent. The term was proposed by the French physiologist A. Dastre in 1893.

Uncoagulated blood was first discovered in the blood vessels of persons who died suddenly by the Italian physician G. Morgagni (1769) and the Scotch anatomist J. Hunter (1794). In 1906 the German researcher P. Morawitz showed that such blood lacks fibrinogen and fibrin. He attributed the absence of these proteins in plasma to the action of a specific enzyme. The enzymatic nature of fibrinolysis was demonstrated by the Soviet scientist V. S. Il’in between 1948 and 1955.

The fibrinolysis system consists of four components: profibrinolysin (or plasminogen), fibrinolysin (or plasmin), profibrinolysin activators, and fibrinolysin inhibitors. Profibrinolysin is converted in the body by the action of enzymatic activators (plasma and tissue activators and urokinase) to fibrinolysin, which under normal physiological conditions is bound by inhibitors—antiplasmins. In certain pathological conditions—thromboses—caused by the breakdown of the clotting mechanism, the bond with the antiplasmins is broken, and fibrinolysin hydrolyzes the fibrin of thrombi. Normally, the activity of the fibrinolysis enzymatic system in the body is low. In the presence of stress, during physical exertion, or after the injection of adrenaline, it may increase sharply. The formation of excessive fibrinolysin by the release of large quantities of tissue activator, resulting from changes in the permeability of blood vessels or injury to them, produces extreme activation of fibrinolysis, which causes bleeding, for example, during obstetrical complications, in cirrhosis of the liver, and during transfusions of incompatible blood. Bleeding is arrested by injection of artificial fibrinolysin inhibitors. A decrease in activity of the fibrinolysis system is associated with the development of atherosclerosis and thromboembolic complications. In such conditions, fibrinolysis is used for thrombolytic therapy.


Andreenko, G. V. Fibrinoliz: Khimiia i fiziologiia protsessa. Moscow, 1967.
Andreenko, G. V. “Sovremennye predstavleniia o sistemakh gemostaza i fibrinoliza.” Klinicheskaia meditsina, 1974, vol. 52.
Kudriashov, B. A. Biologicheskie problemy reguliatsii zhidkogo sostoianiia krovi i ee svertyvaniia. Moscow, 1975.
Astedt, B. “On Fibrinolysis.” Acta Obstetricia et Gynecologica Scandinavica, 1972, no. 51, suppl. 18.
Rickli, E. E. “Human Plasminogen: A Summary of Studies on Its Isolation, Characterization and Activation Mechanism.” Immunochemistry, 1975, vol. 12, nos. 6–7.


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Fibrinolysis is investigated either by the measurement of its individual components (pro- and antifibrinolytic drivers) or through global tests designed to assess the time for clot dissolution upon addition of optimal amounts of tPA.
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Decreased clotting and clot formation time as well as increased fibrinolysis also have a unique TEG tracing, which correlates with the specific hypocoagulable or hypercoagulable state.
However, the diagnosis of fibrinolysis is difficult because of difficulties of laboratory evidence.
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The effects of platelet count on clot retraction and tissue plasminogen activator-induced fibrinolysis on thrombelastography.
t-PA antigen and t-PA activity) appears activated in coordination with the coagulatory system following exercise (14), (17), (18), such that changes in coagulation are generally paralleled by an activation of fibrinolysis to preserve hemostatic balance.
Plasmin participates in fibrinolysis by degrading fibrin and in tissue remodeling by degrading extracellular matrix (ECM) and activating other matrix degrading proteases.
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