急性肺损伤／急性呼吸窘迫综合征中凝血与纤溶研究进展

Research on coagulation and fibrinolysis in acute lung injury and acute respiratory distress syndrome

纤维蛋白沉积有其利与弊。凝血级联活化、纤溶抑制和生理性抗凝物质下调均参与急性肺损伤／急性呼吸窘迫综合征（ALI／ARDS）中纤维蛋白的沉积。三系统功能异常与其基因多态性有关联,微肺不张、死腔增加和炎性因子的表达上调是纤维蛋白沉积的主要致病机制。活化的蛋白C具有抗凝和抗炎的作用，可能有效抑制ALI／ARDS中肺损伤和加速肺纤维化。

Fibrin deposition possesses benefit and harm. Activation of coagulation cascade, inhibition of fibrinolysis,and down-regulation of physiological anticoagulant play a role in fibrin deposition in acute lung injury and acute respiratory distress syndrome （ARDS）. Gene polymorphisms are related to abnormal function of these three systems. Microatelectasis, increase of dead space, and up-regulation of inflammatory cytokines are the major pathopoiesis of fibrin deposition. Activated protein C has anticoagulation and antiinflammatory effect,and may effectively inhibit lung injury and accelerate pulmonary fibrosis in ARDS.