Abstract
Objectives. The aim of this study was to test the effects of collagen external scaffold (CES) in intimal hyperplasia of vein grafts and explore its underlying mechanisms. Methods. Thirty-six New Zealand white rabbits were randomized into no-graft group, graft group, and CES group. The rabbit arteriovenous graft model was established. In CES group, the vein graft was wrapped around with CES. The hemodynamic parameters of vein grafts were measured intraoperatively and 4 weeks after operation by ultrasonic examination. Histological characteristics of vein grafts were also evaluated 4 weeks later. The mRNA and protein levels of proliferating cell nuclear antigen (PCNA), active cleaved-caspase-3 (ClvCasp-3), and smooth muscle 22 alpha (SM22α) were measured 4 weeks later by quantitative real-time PCR and western blot. Results. CES significantly improved the hemodynamic stability of vein grafts, with higher blood velocity and blood flow. Similarly, CES also markedly mitigated intimal hyperplasia and inhibited dilatation of vein grafts. In CES group, the upexpression of PCNA and ClvCasp-3 and the downexpression of SM22α were inhibited. Conclusion. CES exerts beneficial effects in mitigating intimal hyperplasia and improving remodeling of autogenous vein grafts, which may be associated with reducing the proliferation and apoptosis and preserving the phenotype of VSMCs.
Highlights
One million coronary artery bypass grafting (CABG) and peripheral vascular reconstruction procedures are performed around the world each year, and the autologous saphenous vein graft remains the most popular conduit [1]
The vessel wall becomes thicker due to the proliferation of vascular smooth muscle cells (VSMCs) and the deposition of extracellular matrix, both of which contribute to intimal hyperplasia (IH) and vein graft failure [2]
To further investigate the underlying mechanisms, we examined the changes of proliferating cell nuclear antigen (PCNA), ClvCasp-3, and SM22α to observe the proliferation, apoptosis, and phenotypic transition of VSMCs
Summary
One million coronary artery bypass grafting (CABG) and peripheral vascular reconstruction procedures are performed around the world each year, and the autologous saphenous vein graft remains the most popular conduit [1]. The vein grafts undergo necessary “arterialization” to adapt to the arterial circulation. The vessel wall becomes thicker due to the proliferation of vascular smooth muscle cells (VSMCs) and the deposition of extracellular matrix, both of which contribute to intimal hyperplasia (IH) and vein graft failure [2]. Uncontrolled IH may lead to vein graft failure and serious clinical complications. It has been reported that the rate of vein graft failure at 1 and 10 years is approximately 15%–20% and 50%–70%, respectively [3, 4]. Vein graft failure is devastating to individual patients and results in huge healthcare costs
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