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MECHANISMS OF PLATELET ACTIVATION BY BIOMATERIALS AND FLUID SHEAR FLOW

机译:生物材料血小板活化机制和流体剪切流动

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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:心脏病或血管的严重缺陷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更换/克服这些缺陷。然而,将生物材料引入患者的解剖学导致出血和血栓形成并发症。迄今为止,对完全非血栓形成表面的搜索不完整。各种因素占这方面的挑战:我。机械装置的设计因素,尤其是尖锐边缘和连接,引入非生理流动模式,II。基于血管移植物中使用的特定生物材料对生物材料的血液蛋白质反应; III。由于生物材料相互作用,刺激多种途径,其包括蛋白质和细胞水平的相互作用; IV。途径是复杂的,并且互连的扰动单一反应通常不会消除问题; v。触发这些血栓形成过程的确切分子机制仍然没有完全理解。血小板是血液中止血和血栓形成过程的关键蜂窝球员。在本文中,我们描述了由于生物材料相互作用引起的一些血栓形成过程的整体观点,重点是冯维尔布朗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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