Objective: To demonstrate, in a simple and reproducible animal model, that ordinary high viscosity bone cements develop local thrombi; To reduce the occurrence of thrombus in joint arthroplasty, we develop a new material, enoxaparin sodium high viscosity bone cement, to reduce local thrombosis and preliminarily explored the molecular mechanism by which it reduced local thrombus occurrence compared with ordinary high viscosity bone cement. Methods: We used New Zealand rabbits to establish two groups of animal models: ordinary high viscosity bone cement group and new enoxaparin sodium high viscosity bone cement group on the basis of carotid artery vein extracorporeal shunt. There were 3 rabbits in each group. The experimental samples were collected 4 hours after modeling, and the amount of thrombosis between the two groups was compared, The collected vascular tissue samples were quantitatively detected for endothelial cell related thrombomodulin.Results: we successfully established the animal model on the basis of arteriovenous shunt in New Zealand rabbits. We found that both ordinary high viscosity bone cement and new enoxaparin sodium high viscosity bone cement could form thrombosis. The weight of thrombosis in ordinary high viscosity bone cement group was 0.00706 ± 0.00136g/cm, The weight of thrombosis in the new enoxaparin sodium high viscosity bone cement group was 0.00551 ± 0.00115g/cm. The amount of thrombosis in the new enoxaparin sodium high viscosity bone cement group was significantly reduced. We detected by RT qPCR and Western blot that the expression of CD40, a related protein that can regulate thrombosis in vascular endothelial cells, was significantly lower in the new enoxaparin sodium high viscosity bone cement group than that in the normal high viscosity bone cement group.Conclusion: We confirm that the new enoxaparin sodium high viscosity bone cement forms less thrombus than common high viscosity bone cement and preliminarily elucidate that the molecular mechanism by which this new material reduces thrombus formation is to decrease the expression of thrombus associated regulatory protein CD40 in vascular endothelial cells.