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Streptokinase is a thrombolytic medication activating plasminogen by nonenzymatic mechanism. [1] As a medication it is used to break down clots in some cases of myocardial infarction (heart attack), pulmonary embolism, and arterial thromboembolism. [2]
Streptococcus canis is a group G beta-hemolytic species of Streptococcus. [1] It was first isolated in dogs, giving the bacterium its name. These bacteria are characteristically different from Streptococcus dysgalactiae, which is a human-specific group G species that has a different phenotypic chemical composition.
The clot consists of platelets interconnected by the clotting protein fibrin. As the clot matures, the fibrin content increases and the clot may exhibit stratification. [7] Even in healthy animals, injuries to the endothelium occur spontaneously from time to time, but there is a balance between thrombus formation and breakdown.
Binding clots or cell surfaces cause their conformation to change, allowing them to be activated by plasminogen activators. Plasminogen activators do so by cleaving the R561/V562 peptide bond, producing the active protein plasmin, which catalyzes the degradation of fibrin polymers that make up the structure of blood clots.
However, streptokinase causes systemic fibrinolytic state and can lead to bleeding problems. Tissue plasminogen activator (tPA) is a different enzyme that promotes the degradation of fibrin in clots but not free fibrinogen. [14] This drug is made by transgenic bacteria and converts plasminogen into the clot-dissolving enzyme, plasmin. [15]
An anticoagulant, commonly known as a blood thinner, is a chemical substance that prevents or reduces the coagulation of blood, prolonging the clotting time. [1] Some occur naturally in blood-eating animals, such as leeches and mosquitoes, which help keep the bite area unclotted long enough for the animal to obtain blood.
Tissue-type plasminogen activator, short name tPA, is a protein that facilitates the breakdown of blood clots. It acts as an enzyme to convert plasminogen into its active form plasmin, the major enzyme responsible for clot breakdown.
The treatments to prevent the formation of blood clots is balanced against the risk of bleeding. [5] One of the goals of blood clot prevention is to limit venous stasis as this is a significant risk factor for forming blood clots in the deep veins of the legs. [6] Venous stasis can occur during the long periods of not moving.
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