Factor XI‐deficient mice exhibit increased bleeding after injury to the saphenous vein

Abstract

Background Factor XI (FXI) is a key component of the intrinsic pathway of coagulation. It can be activated by either FXIIa or thrombin and amplifies thrombin generation during clot formation. Congenital FXI deficiency in humans (known as hemophilia C) is associated with bleeding after hemostatic challenge. However, to date there are no reports of excess bleeding in FXI-deficient mice. Objectives To determine if the absence of FXI in mice prolongs bleeding in different models. Methods We assessed the hemostatic capacity of FXI-/- mice in three different bleeding models: tail bleeding, surgical bleeding and saphenous vein bleeding. Results We found that tail bleeding and surgical bleeding of FXI-/- mice were similar to wild-type mice. However, FXI-/- mice had an impaired hemostatic capacity in the saphenous vein bleeding model compared with wild-type controls. Conclusions Our results indicate that FXI-/- mice have a mild hemostatic defect after injury to the saphenous vein but not after transection of the tail or vessels in the abdominal wall.