| Acute lung injury (ALI) and acute respiratory distress
syndrome (ARDS) are common, life-threatening causes of acute respiratory
failure that arise from a variety of local and systemic insults. The need
for new specific therapies has led a number of investigators to examine
the role of altered coagulation and fibrinolysis in the pathogenesis of
ALI/ARDS. This review summarizes our current understanding of coagulation
and fibrinolysis in human ALI/ARDS with an emphasis on pathways that could
be potential therapeutic targets including the tissue factor pathway, the
protein C pathway and modulation of fibrinolysis via plasminogen activator
inhibitor-1. The available data suggest that clinical ALI and ARDS are characterized
by profound alterations in both systemic and intra-alveolar coagulation
and fibrinolysis. Fibrin deposition in the airspaces and lung microvasculature
likely results from both activation of the coagulation cascade and impaired
fibrinolysis, triggered by inflammation. Modulation of fibrin deposition
in the lung through targeting activation and modulation of coagulation as
well as fibrinolysis may be an important therapeutic target in clinical
ALI/ARDS that deserves further exploration. |
