Fibrinolysis

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fibrinolysis

[‚fī·brə′näl·ə·səs]
(physiology)
Liquefaction of coagulated blood by the action of plasmin on fibrin.

Fibrinolysis

 

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.

REFERENCES

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.

G. V. ANDREENKO

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Only 3 patients received a fibrinolytic agent within 1 hour, 34 did so between 1 and 12 hours, and 63 either did not receive a fibrinolytic therapy at all or received it after 12 hours.
At SBAH, after assessment by a doctor, 60% received a fibrinolytic agent within 1 hour of assessment, with 41% receiving the medication after more than 1 hour.
Furthermore, the first attending doctor who was appropriately able to administer a fibrinolytic agent generally did not do so.
33 (33-74) Men, n (%) 131 (85) Medical history Hypertension, n (%) 55 (35) Diabetes, n (%) 46 (30) Dyslipidemia, n (%) 26(17) Presentation Chest pain, n (%) 147 (95) Anterior location, n (%) 77 (50) Fibrinolytic agent Streptokinase, n (%) 7 (4.
1,3,11-13) Because blood clots often obstruct the external ventriculostomies, however, there are significant technical difficulties associated with this procedure, (1,3,11-13) Several investigators have reported the use of various fibrinolytic agents in the management of this problem, with varying results.
Fibrinolytic agents (urokinase, rt-PA, streptokinase) have been used in the treatment of lysis of intraparenchymal hematomas, (30) posthemorrhagic hydrocephalus in preterm infants, (31,32) IVH in preterm infants, (31,32) lysis of cisternal clots associated with aneurysmal subarachnoid hemorrhage, (33,34) and IVH of various etiologies in adults.
The rationale for using rt-PA for intraventricular blood clot lysis has been adequately described by Goh and Poon (14): rt-PA is thought to enhance the normal fibrinolytic process within the CSF pathways and therefore can be considered more physiologic than the previously used fibrinolytic agents (eg, urokinase).
The use of fibrinolytic agents in the treatment of IVH has been occasionally associated with serious side effects.
Fibrinolytic agents in the treatment of intraventricular hemorrhage in adults.
The study evaluated the combination of half the standard dose of the clot-dissolving fibrinolytic agent RETAVASE(R) (reteplase) and a standard dose of ReoPro(R) (abciximab), a drug that prevents the formation of blood clots, as a potential new treatment regimen for heart attack.
Retavase, a fibrinolytic agent, has been approved for marketing by the regulatory authorities in Canada and will soon be available to hospitals nationwide.