Heparin can also promote with endothelial tissue factor via bay (TFPI)
release, TFPI and factor X a combination and inactivated Xa, constitute the
TFPI/factor Xa compound, the compound within the TFPI and then inactivated and
tissue factor Ⅶ a combination of factors.
Heparin sodium, a manufacturer of heparin sodium, can suppress the thrombus formation caused by endothelial injury and atherosclinal plaque rupture through this way, which may be the main mechanism of heparin sodium drugs to prevent thrombus formation.
The anticoagulant activity and eradication rate of heparin sodium are affected by the chain length. High molecular weight fragments were removed from the cycle faster than low molecular weight fragments, resulting in increased accumulation of low molecular weight fragments and decreased resistance to IIa/Xa ratios.
In vitro, heparin sodium combined with platelets can induce or suppress platelet aggregation according to different test conditions.
Heparin sodium activates heparin sodium cofactor II and directly inactivates coagulation factor IIa. The effect is charge-dependent, independent of pentose structure, and requires a higher heparin sodium concentration. The inactivation of IIa factor mediated by heparin sodium cofactor II is also dependent on relative molecular weight, requiring at least 24 sugar units (relative molecular weight above 7200). This mechanism of heparin sodium can come into play in severe AT deficiency.