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Effects of anticoagulant strategies on activation of inflammation and coagulation.

机译:抗凝策略对炎症和凝血激活的影响。

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摘要

Acute inflammatory events, such as those that occur in sepsis, lead to dysregulation of the coagulation cascade. The hemostatic imbalance in sepsis, characterized by the excessive activation of procoagulant pathways and the impairment of anticoagulant activity, leads to disseminated intravascular coagulation and results in microvascular thrombosis, tissue hypoperfusion and, ultimately, multiple organ failure and death. Furthermore, natural anti-inflammatory mechanisms of the endogenous anticoagulants are diminished by the impaired coagulation. Supportive strategies aiming at inhibiting activation of coagulation and inflammation by treatment with exogenous anticoagulants have been found to be beneficial in experimental and initial clinical studies. This review summarizes the available experimental and clinical data regarding the interaction between coagulation and inflammation, focusing on the two anticoagulants which are in clinical use, antithrombin and activated protein C. Identification of the different biological mechanisms of the two endogenous anticoagulants might help to determine target patient populations as well as to develop new anticoagulant analogs that differ in there respective effects in coagulation and inflammation.
机译:急性炎症事件(例如败血症中发生的事件)导致凝血级联失调。脓毒症中的止血失衡,其特征在于促凝血途径的过度激活和抗凝活性的损害,导致弥散性血管内凝血,并导致微血管血栓形成,组织灌注不足,并最终导致多器官衰竭和死亡。此外,内源性抗凝剂的天然抗炎机制因凝血受损而减弱。已经发现旨在通过用外源性抗凝剂治疗来抑制凝血和炎症活化的支持策略在实验和初始临床研究中是有益的。这篇综述总结了有关凝血与炎症之间相互作用的可用实验和临床数据,重点是临床上使用的两种抗凝剂,即抗凝血酶和活化蛋白C。鉴定两种内源性抗凝剂的不同生物学机制可能有助于确定靶点患者群体以及开发新的抗凝血类似物,它们在凝血和炎症方面的作用不同。

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