Heparin promotes the release of endothelium-bound tissue factor pathway repressor TFPI, which binds to factor Xa and inactivates Xa to form the TFPI/factor Xa complex, in which TFPI inactivates the tissue factor-bound factor Ⅶ A.
Heparins Manufacturer introduced that heparin sodium can inhibit the thrombosis formation caused by endothelial injury and atheromatous plaque rupture through this pathway, which may be the main mechanism of heparin sodium to prevent thrombosis formation.
The anticoagulant activity and eradication rate of heparin sodium were affected by the chain length. The higher molecular weight fragments were removed from the circulation faster than the lower molecular weight fragments, which increased the accumulation of the lower molecular weight fragments and decreased the anti-IIA/Xa ratio.
In vitro, heparin binding platelet can induce or inhibit platelet aggregation according to different experimental conditions.
Heparin activates heparin cofactor Ⅱ and directly inactivates clotting factor Fla A. The effect is charge - dependent, independent of the pentose structure, and requires a higher concentration of heparin. Heparin cofactor Ⅱ mediated inactivation of clotting factor FLAA is relative molecular mass dependent, requiring at least 24 sugar units (relative molecular mass over 7200). This mechanism of heparin can be activated in severe AT deficiency.