【Objective】 To establish a venous bypass graft arteriosclerotic mouse model for exploring the mechanisms of vascular remodeling induced by blood pressure-related mechanical stress. 【Methods】 The right common carotid arteries of anesthetic 11-12 week-old C57BL/6J mice were cut in the middle

and polyethylene cuffs were placed at both ends of the arteries. Then the supradiaphragmatic vena cava from isogenic littermate donor mice were harvested and grafted as interposition grafts. Morphometric assessments including H&E staining

Ponceau-Vitoria-blue staining and immunohistochemistry were performed on paraffin-embeded sections of the vein grafts harvested 2 weeks

4 weeks

8 weeks after surgery. 【Results】 The grafted veins in response to carotid artery pressure demonstrated remarkably increased vessel wall thickness in a time-dependent manner. The neointima of the veins grafted 8 w increased about 8 folds than that of normal vein control[(88.97 ± 16) μm vs (11.10 ± 0.9)μm

P < 0.01)]. Furthermore

significant proliferation of vascular smooth muscle cells (α-actin+) could be seen in the neointimal lesions increasing at 2 weeks postsurgery

reaching peak at 4 weeks and then decreasing at 8 weeks with increased extracellular matrix. In addition

the elastic membranes of the grafted veins underwent fragmentation

synthesis and reorganization from 2 weeks to 8 weeks after grafting.【Conclusions】 Increased blood pressure-initiated mechanical stress can directly induce mouse venous bypass graft artherosclerosis and elastic membrane remodeling. The study would provide a novel animal model for exploring molecular mechanisms of vascular remodeling and prevention and treatment of hypertension.