Pharmacological action of heparin sodium：
Heparin is a mixture of aminoglucosides. The main repeating structure in the molecule is disaccharide trisulfate chain, only a few disaccharides form pentose sequence chain. Anticoagulant effect depends on the heparin five sequences of sugar chain groups in several sulfate and antithrombin Ⅲ (AT Ⅲ) affinity. Heparin as auxiliary factor, can enhance the AT Ⅲ and activation of clotting factors such as Ⅱ a, Ⅸ a and Ⅺ a, a, Ⅹ Ⅻ a and the role of fibrinolytic enzyme.
Therefore, heparin has an effect on many aspects of the coagulation process. The mechanism of heparin action has not been fully elucidated. Now that heparin and AT Ⅲ to depress complex electronic bonds form. The formation of the complex changes AT Ⅲ configuration, exposed the activation center, can make AT Ⅲ and serine protease, the activation center form irreversible covalent bonds combined with 1:1 stoichiometric compounds, serine protease was inactivated in the process. The formation of covalent bonds to the AT Ⅲ of heparin affinity is abate, heparin can be release.
Plasma concentrations of heparin acceleration AT Ⅲ activation theory only 0.01 u/ml. If the plasma heparin level was >11u/ml, the reaction rate was increased by 2000 times, and the plasma thrombin t1/2<40 seconds was shortened to 0.01 seconds. Heparin was not consumed during this process. Low-dose heparin anticoagulant effect is mainly due to neutralize Ⅹ F a, thereby blocking prothrombin into thrombin. In the case of low dose heparin, the neutralization ability of thrombin is low. Therefore, low dose heparin has a low degree of anti-thrombotic function by inhibiting the production of thrombin before the complete production of thrombin. It is mainly suitable to inhibit thrombin production under the condition of blood stasis, as a preventive application.
Enough and thrombin in heparin therapy (Ⅱ a) to prevent fibrinogen into fibrin. Full amount and heparin can inhibit blood coagulation beginning phase generated by thrombin and fibrin stability factor F Ⅷ activation, prevent stable fibrin clot formation; Inhibit Ⅱ a influence on platelet aggregation, inhibit Ⅴ F and F Ⅷ activation and effective anticoagulant effect.
Heparin has no thrombolytic effect and cannot dissolve the formed blood clot. The difference between heparin and oral anticoagulant is that the anticoagulant action is rapid, both in vivo and in vitro have anticoagulant activity. Other effects: Heparin has a lipid-lowering effect in vivo, mainly because it stimulates the release and activation of lipoprotein esterase and hydrolyzes the triacylglycerol of Chylous granule into fatty acid and glycerol, and makes the plasma of chylous granule with lipidemia clear. The dose of heparin required for the lipid-lowering effect is lower than the anticoagulant amount, but it has been reported that the use of heparin for a period of time causes hyperlipidemia rebound.