Heparin effect in alveolar cells and macrophages in an acute lung injury model.

Introduction Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS) are characterized by a promptly release of proinflammatory mediators that downregulate natural anticoagulant mechanisms, initiate the coagulation system, impair fibrinolysis and produce the rupture of the endothelial and epithelial monolayer [1]. Inflammation of ALI/ARDS is initiated and strongly regulated by proinflammatory activation of macrophages, which lead to the recruitment of other inflammatory cells, producing alveolar cells injury, propagating the coagulant response and promoting the injury. Currently there is no effective treatment for this disease. Previous studies have presented the beneficial effect of anticoagulants, not only for their anticoagulation activity but also for their antiinflammatory action [2],[3].