Anticoagulants generally inhibit the appearance of fibrin filaments; they prevent thrombus formation, help to stop the growth of already formed thrombi, enhance the effect on thrombi of endogenous fibrinolytic enzymes.
Anticoagulants are divided into 2 groups: a) direct anticoagulants – fast acting (sodium heparin, calcium nadroparin, sodium enoxaparin, etc.), effective in vitro and in vivo; b) indirect anti-coagulants (vitamin K antagonists) – long-acting (warfarin, phenindione, acenocoumarol, etc.), act only in vivo and after the latency period.
The anticoagulant effect of heparin is associated with a direct effect on the blood coagulation system due to the formation of complexes with many factors of hemocoagulation and is manifested in the inhibition of phases I, II and III of coagulation. Heparin itself is activated only in the presence of antithrombin III.
Indirect anticoagulants – derivatives of oxycoumarin, indandione, competitively inhibit vitamin K reductase, thereby inhibiting the activation of the latter in the body and stopping the synthesis of K-vitamin-dependent plasma hemostasis factors – II, VII, IX, X.
Below is a list of anticoagulants:
- Antithrombin III
- Enoxaparin sodium
- Fondaparinux sodium
- Heparin sodium
- Heparinoid (Heparinoidum)
- Drotrecogin alpha (activated)
- Heparinum calcium
- Reviparin sodium
- Nadroparin calcium
- Sodium citrate (Natrii citras)
- Ethyl biscumacetate
- Leech powder (Pulvis hirudinum)
- Dabigatran etexilate
- Protein C human (Proteinum C humanum)
- Certoparin sodium
- Parnaparin sodium
- Dalteparin sodium
- Bemiparin sodium
- Dextrose + Citric acid + Sodium dihydrophosphate + Sodium citrate (Dextrosum + Acidum citricum + Natrii dihydrophosphas + Natrii citras)