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MECHANISMS OF PLATELET ACTIVATION BY BIOMATERIALS AND FLUID SHEAR FLOW

机译:生物材料和流体剪切流活化血小板的机理

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Severe defects in the heart or blood vessels leads to various cardiovascular diseases (CVD) and patients sometimes require biomaterial based implants to replace/overcome these defects. However, introduction of biomaterials into the patient's anatomy leads to bleeding and thrombosis complications. To date, the search for a completely non-thrombogenic surface is not complete. Various factors account for the challenges found in this regard: ⅰ. design factors of mechanical devices, especially at the sharp edges and connections, introduce non-physiological flow patterns, ⅱ. blood protein responses to the biomaterial vary based on the specific biomaterial used in the vascular grafts; ⅲ. multiple pathways are stimulated due to biomaterial-blood interactions which include interactions both at the protein and the cellular levels; ⅳ. the pathways are intricate and inter-linked due to which perturbing a single reaction does not usually eliminate the problem; and ⅴ. the exact molecular mechanisms that trigger these thrombogenic processes is still not fully understood. Platelets are the key cellular players in both the hemostatic and thrombotic processes in blood. In this review, we describe an overall view of some of the thrombogenic processes initiated due to biomaterial-blood interactions, with focus on the role of von Willebrand factor in shear induced platelet activation and aggregation processes.
机译:心脏或血管中的严重缺陷会导致各种心血管疾病(CVD),患者有时需要基于生物材料的植入物来替代/克服这些缺陷。然而,将生物材料引入患者的解剖结构会导致出血和血栓形成并发症。迄今为止,对完全不具有血栓形成作用的表面的搜索尚未完成。各种因素导致了这方面的挑战:ⅰ。机械设备的设计因素,特别是在尖锐的边缘和连接处,会引入非生理性的流动模式,。血液对生物材料的蛋白质反应因血管移植物中使用的特定生物材料而异; ⅲ。由于生物材料与血液的相互作用(包括蛋白质和细胞水平的相互作用),刺激了多种途径; ⅳ。这些途径是错综复杂的和相互联系的,因此干扰单个反应通常不能消除问题。和ⅴ。引发这些血栓形成过程的确切分子机制仍不完全清楚。血小板是血液止血和血栓形成过程中的关键细胞因子。在这篇综述中,我们描述了由于生物材料-血液相互作用而引发的某些血栓形成过程的总体观点,重点是冯·威兰布兰德因子在剪切诱导的血小板活化和聚集过程中的作用。

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