Objective : To investigate the mechanisms underlying restenosis following coronary artery bypass grafting using bridging veins.Method : We established a rabbit model of venous arterialisation, by transplanting veins into the arterial system as bridging vessels and investigated vessel tensile mechanical and histomorphological properties. Result : Control vein elasticity (k = 16.20) was less than that of the control artery (k = 58.04; P < 0.05), and vein walls were thinner. Following venous arterialisation, proliferating cell nuclear antigen and alpha-actin were upregulated and vein walls thickened (P < 0.05), with elasticity after venous arterialisation (k = 86.26) significantly higher than that of control veins (P < 0.05). Conclusion : This indicates that venous intima is damaged by high pressure following arterialisation, resulting in gradual restenosis, with thickening of the venous intima and an increase in vessel elasticity. Clinically, there is potential to repeat these experiments to determine the elastic extremum of the great saphenous vein and control the pressure in the lumen of this vessel, to ensure minimal damage to the intima before anastomosis, thereby facilitating improvement of long-term patency rates following vein bridge surgery. Whether the increase in venous bridge elasticity after venous arterialisation can be controlled, with the aim of preventing early-stage restenosis, warrants investigation.
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