Heparin sodium can also promote the release of endothelium-bound tissue factor through the inhibitor (TFPI), which binds to factor Xa and inactivates Xa to form the TFPI/factor Xa complex, in which TFPI then inactivates the tissue factor-bound factor Ⅶ A.

　　The Heparins Manufacturer say that in this way heparin inhibits the formation of thrombus caused by endothelial injury and atheromatous plaque rupture, which may be the main mechanism by which heparin drugs prevent thrombus 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 sodium binds to its own platelets, inducing or suppressing platelet aggregation, depending on the development of the study.

　　Heparin sodium activates heparin cofactor II and directly inactivates coagulation factor IIA. This effect is charge dependent, independent of the pentose structure, and requires higher heparin sodium concentration. Heparin sodium cofactor II mediated inactivation of factor IIA is also relative molecular weight dependent, requiring at least 24 sugar units (relative molecular weight over 7200). This mechanism of heparin sodium may play a role in severe AT deficiency.