Dynamic Luminal Topography: A Potential Strategy to Prevent Vascular Graft Thrombosis

动态管腔形貌:预防血管移植血栓形成的潜在策略

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Abstract

AIM: Biologic interfaces play important roles in tissue function. The vascular lumen-blood interface represents a surface where dynamic interactions between the endothelium and circulating blood cells are critical in preventing thrombosis. The arterial lumen possesses a uniform wrinkled surface determined by the underlying internal elastic lamina. The function of this structure is not known, but computational analyses of artificial surfaces with dynamic topography, oscillating between smooth and wrinkled configurations, support the ability of this surface structure to shed adherent material (Genzer and Groenewold, 2006; Bixler and Bhushan, 2012; Li et al., 2014). We hypothesized that incorporating a luminal surface capable of cyclical wrinkling/flattening during the cardiac cycle into vascular graft technology may represent a novel mechanism of resisting platelet adhesion and thrombosis. METHODS AND RESULTS: Bilayer silicone grafts possessing luminal corrugations that cyclically wrinkle and flatten during pulsatile flow were fabricated based on material strain mismatch. When placed into a pulsatile flow circuit with activated platelets, these grafts exhibited significantly reduced platelet deposition compared to grafts with smooth luminal surfaces. Constrained wrinkled grafts with static topography during pulsatile flow were more susceptible to platelet accumulation than dynamic wrinkled grafts and behaved similar to the smooth grafts under pulsatile flow. Wrinkled grafts under continuous flow conditions also exhibited marked increases in platelet accumulation. CONCLUSION: These findings provide evidence that grafts with dynamic luminal topography resist platelet accumulation and support the application of this structure in vascular graft technology to improve the performance of prosthetic grafts. They also suggest that this corrugated structure in arteries may represent an inherent, self-cleaning mechanism in the vasculature.

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