Abstract：
Sepsis and septic shock result from an inadequate host response to an infection, which causes organ dysfunction. The progression of this condition is manifested by the occurrence of successive clinical stages, resulting from the systemic inflammatory response secondary to the activation of different inflammatory mediators, leading to organ dysfunction. There is a high burden of evidence on the role of endotoxin in the pathogenesis of sepsis and its crucial role in triggering the inflammatory response in sepsis caused by gram-negative bacteria. The coagulation cascade activation in sepsis patients is part of the host\'s adaptive immune response to infection. The endothelium is the main target in sepsis, which is metabolically active and can.
摘要：
败血症和脓毒性休克是宿主对感染反应不足的结果，导致器官功能障碍.这种情况的进展表现为连续临床阶段的发生，由继发于不同炎症介质激活的全身炎症反应引起，导致器官功能障碍.关于内毒素在脓毒症的发病机理中的作用及其在引发革兰氏阴性菌引起的脓毒症炎症反应中的关键作用，有大量证据。脓毒症患者的凝血级联激活是宿主对感染的适应性免疫反应的一部分。内皮是脓毒症的主要靶点,代谢活跃，可以。
