Heterozygous antithrombin deficiency improves in vivo haemostasis in factor VIII-deficient mice.

摘要: Decreased levels of factor VIII (FVIII) limit the amount thrombin generated at site injury, but not rate that is neutralised by antithrombin (AT). We hypothesised FVIII-deficient mice with heterozygous AT deficiency will demonstrate increased generation and therefore less in vivo bleeding compared to normal levels. Therefore, we performed tail experiments wild-type (WT), deficient (AT+/-) mice, (FVIII-/-) (FVIII-/-/AT+/-). Amount was assessed measuring absorbance haemoglobin released from lysed red blood cells collected after transection. In addition, measured generation, activated partial thromboplastin time (aPTT), activity plasma different groups. Tail significantly reduced FVIII-/-/AT+/- FVIII-/- mice. On other hand, there no difference between AT+/- Thrombin dependent on genotype, following order: < WT AT+/-. The aPTT influenced (i.e. genotype), prolonged Using as an murine model demonstrated moderately increase decrease traumatic vessel injury. agreement congenital thrombotic conditions, our data elucidate phenotypes can be modulated balance procoagulant anticoagulant proteins.