|Heparin works by potentiating the action of antithrombin III, as it is similar to the heparan sulfate proteoglycans which are naturally present on the cell membrane of the endothelium. It decreases the rate of coagulation by increasing the rate at which antithrombin III, inhibits activated coagulation factors, particularly thrombin, a key enzyme in the coagulation cascade. Because antithrombin III
inactivates many coagulation proteins, the process of coagulation will slow down. Heparin exhibits a variety of biological activities. Heparin binds to a wide variety of cell growth factors, cytokines and cell adhesion molecules.
Heparin is often used as a treatment for certain blood vessel, heart, and lung conditions. Heparin will not dissolve blood clots that have already formed, but it may prevent the clots from becoming larger and causing more serious problems. Heparin has been used for already a long time as an anticoagulant and antithrombotic agent in the treatment and prevention of venous thrombosis. Heparin is also used to prevent blood clotting during open-heart surgery, bypass surgery, and dialysis. Heparin is widely used as an anticoagulant in conjunction with invasive surgical procedures and dialysis procedures, to prevent clotting in intravenous lines and in the treatment of thrombolytic disorders. Heparin has been used in surgery of the heart and blood vessels, with organ transplants and artificial organs, for cardiovascular diagostic techniques, and for the control and prevention of thromboembolism following surgical operations. At the conclusion of these procedures, the anticoagulation effects of heparin must be neutralized or reversed in order to prevent the patient from bleeding.
Heparin protection of cellular destruction and enhancement of revascularization and heparin induced epithelialization and re-epithelialization can be favorably applied to treat dermatitides, fissures, and fistulas that are difficult to heal, or are refractory to current methods of treatment. Heparin by itself (without a steroid) enhances the intensity of angiogenesis induced by tumors and by tumor derived factors in vivo, although in the absence of tumor cells or tumor extracts or tumor derived factors neither heparin nor the mast cells which release heparin could induce angiogenesis.