期刊
CRITICAL CARE MEDICINE
卷 31, 期 4, 页码 S238-S242出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.CCM.0000057849.53689.65
关键词
acute lung injury; antithrombin; bronchoalveolar fluid; coagulation; cytokines; fibrinolysis; plasminogen activator; plasminogen activator inhibitor; protein C; sepsis; thrombin; tissue factor; tissue factor pathway inhibitor
Objectives: To review the involvement of coagulation and fibrinolysis in the pathogenesis of acute lung injury during severe infection. To review the cross-talk between coagulation and inflammation that may affect this response. Data Sources: Published articles on experimental and clinical studies of coagulation and fibrinolysis during infection, inflammation, acute lung injury, and evolving acute respiratory distress syndrome. Conclusions: Fibrin deposition is an important feature of pulmonary infection or severe inflammation. The mechanisms that contribute to this fibrin deposition are bronchoalveolar tissue factor-mediated thrombin generation and localized depression of urokinase plasminogen activator-mediated fibrinolysis, caused by the increase of plasminogen activator inhibitors. These effects on pulmonary coagulation and fibrinolysis are regulated by various proinflammatory cytokines. Rather than being a unidirectional relationship, the interaction between inflammation and coagulation involves significant cross-talk. Coagulation and fibrinolytic proteins may have an additional role beyond fibrin turnover and inflammation, e.g., in mechanisms mediating cell recruitment and migration.
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