Unihepa Mechanism of Action

Pharmacology: Pharmacodynamics: Heparin is a naturally occurring mucopolysaccharide which inhibits the clotting of blood in vitro and in vivo. It enhances the rate at which antithrombin III neutralises thrombin and activated factor X (X_a). Antithrombin III also neutralises other activated coagulation factors, eg. factors IX, XI, XII and plasmin.
With low-dose heparin therapy, anticoagulation appears to result from neutralisation X_a which prevents the conversion of prothrombin to thrombin. With full-dose heparin therapy, anticoagulation appears to result primarily from neutralisation of thrombin which prevents the conversion of fibrinogen to fibrin. Full-dose heparin therapy also prevents the formation of a stable fibrin clot by inhibiting activation of fibrin stabilising factor.
Pharmacokinetics: Heparin is not absorbed from the gastrointestinal tract and must be administered parenterally. Its onset of action is immediate following I.V. administration. There may be considerable variation among patients in the extent of absorption following deep subcutaneous injection of heparin; however, the onset of activity usually occurs within 20-60 minutes.
Heparin is extensively bound to plasma proteins. It does not cross the placenta and is not distributed into milk.
The metabolic fate of heparin is not fully understood. No biotransformation in plasma or liver, nor any renal excretory mechanism has been identified as primarily responsible for elimination of the drug. It has been suggested that transfer and storage in the reticuloendothelial system may play a role, or that heparin may be partially metabolised in the liver. After administration of large doses intravenously, a small fraction of unchanged drug is excreted in the urine.