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Alterations in platelet behavior after major trauma: adaptive or maladaptive?

机译:主要创伤后的血小板行为的变化:适应性或适应性?

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摘要

Platelets are damage sentinels of the intravascular compartment, initiating and coordinating the primary response to tissue injury. Severe trauma and hemorrhage induce profound alterations in platelet behavior. During the acute post-injury phase, platelets develop a state of impaired ex vivo agonist responsiveness independent of platelet count, associated with systemic coagulopathy and mortality risk. In patients surviving the initial insult, platelets become hyper-responsive, associated with increased risk of thrombotic events. Beyond coagulation, platelets constitute part of a sterile inflammatory response to injury: both directly through release of immunomodulatory molecules, and indirectly through modifying behavior of innate leukocytes. Both procoagulant and proinflammatory aspects have implications for secondary organ injury and multiple-organ dysfunction syndromes. This review details our current understanding of adaptive and maladaptive alterations in platelet biology induced by severe trauma, mechanisms underlying these alterations, potential platelet-focused therapies, and existing knowledge gaps and their research implications.
机译:血小板是血管内腔室的损伤前哨细胞,启动并协调组织损伤的主要反应。严重的创伤和出血会引起血小板行为的深刻改变。在急性损伤后阶段,血小板形成一种不依赖于血小板计数的体外激动剂反应性受损状态,与系统性凝血病和死亡风险相关。在最初的损伤中存活下来的患者,血小板变得高度反应,与血栓事件的风险增加相关。除了凝血之外,血小板还构成了对损伤的无菌炎症反应的一部分:直接通过释放免疫调节分子,间接通过改变固有白细胞的行为。促凝和促炎因素对继发性器官损伤和多器官功能障碍综合征均有影响。这篇综述详细介绍了我们目前对严重创伤引起的血小板生物学适应性和不适应性改变的理解,这些改变的机制,潜在的以血小板为中心的治疗,以及现有的知识差距及其研究意义。

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