Heparin¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ The mechanism of action of heparin is antithrombin-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of heparin is well correlated to the inhibition of factor Xa. Heparin interacts with antithrombin III, prothrombin and factor X.
Pharmacology
Heparin¿¡ ´ëÇÑ Pharmacology Á¤º¸ Heparin is a highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Heparin is a well known and commonly used anticoagulant which has antithrombotic properties. Heparin is indicated for the prophylaxis of deep vein thrombosis, which may lead to pulmonary embolism, and also for the prophylaxis of ischemic complications of unstable angina and non-Q-wave myocardial infarction, when concurrently administered with aspirin. Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo. Heparin acts at multiple sites in the normal coagulation system. Small amounts of Heparin in combination with antithrombin III (Heparin cofactor) can inhibit thrombosis by inactivating activated Factor X and inhibiting the conversion of prothrombin to thrombin. Once active thrombosis has developed, larger amounts of heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Heparin also prevents the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilizing factor.
Metabolism
Heparin¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
Protein Binding
Heparin¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Very high, mostly to low-density lipoproteins
Half-life
Heparin¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 1.5 hours
Absorption
Heparin¿¡ ´ëÇÑ Absorption Á¤º¸ Some oral absorption but lack of anticoagulant effect. Rapidly taken up by endothelial cells with remainder bound to plasma proteins.
Biotransformation
Heparin¿¡ ´ëÇÑ Biotransformation Á¤º¸ Liver and the reticulo-endothelial system are the sites of biotransformation.
Toxicity
Heparin¿¡ ´ëÇÑ Toxicity Á¤º¸ Heparin sodium - Mouse, median lethal dose greater than 5000 mg/kg. Another side effect is heparin induced thrombocytopenia (HIT syndrome). HIT is caused by an immunological reaction that makes platelets form clots within the blood vessels, thereby using up coagulation factors
Drug Interactions
Heparin¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Aspirin Association of ASA/Heparin increases risk of bleedingDrospirenone Increased risk of hyperkaliemia
Heparin¿¡ ´ëÇÑ Description Á¤º¸ Heparin, a highly sulfated glycosaminoglycan is widely used as an injectable anticoagulant. It has the highest negative charge density of any known biological molecule. Heparin acts as an anticoagulant, preventing the formation of clots and extension of existing clots within the blood. While heparin does not break down clots that have already formed, it allows the body's natural clot lysis mechanisms to work normally to break down clots that have already formed. Heparin binds to and accelerates the activity of antithrombin III. By activating antithrombin III, heparin preferentially potentiates the inhibition of coagulation factors Xa and IIa. Factor Xa catalyzes the conversion of prothrombin to thrombin, so heparin? s inhibition of this process results in decreased thrombin and ultimately the prevention of fibrin clot formation.