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Background  Acute lung injury (ALI) induces a coagulation/fibrinolysis imbalance and leads to fibrin deposition. The protein C pathway is an important regulator of the coagulation system and reduces the inflammatory response. The aim of the study was to examine the effects of recombinant human activated protein C (rhAPC) in the early phase of  Pseudomonas aeruginosa  ( Pa )-induced lung injury.    Methods  The study was conducted in vivo on a rat model of  Pa -induced ALI. Continuous intravenous (IV) rhAPC was administrated simultaneously with intratracheal (IT)  Pa . We instilled into the airspaces a 5% bovine albumin solution with 1 μ(Ci of  125  I-albumin and injected IV 1 μ(Ci of  111 In-albumin to measure lung liquid clearance (LLC) and endothelial injury. Cytokines levels (TNFα and IL-6) and thrombin-antithrombin (TAT) complexes were measured in blood and bronchoalveolar lavage fluid (BALF) at 4 hours. Four groups were compared: control (CTR), pneumonia (PNP) receiving IT  Pa  (0.5 ml/kg of 1 × 10 9  cfu), APC: IV rhAPC (300 μg/kg/h), A-PNP: IT  Pa  /IV rhAPC.    Results  Alveolar-capillary permeability was increased in the PNP versus the CTR group (0.28 ± 0.08 vs. 0.03 ± 0.01, p < 0.05). IV rhAPC in  Pa -induced ALI led to further injury (0.47 ± 0.17 vs. 0.28 ± 0.08, p = 0.2). The LLC was significantly decreased in the A-PNP group compared to PNP group (9.1 ± (4.3% vs. 33.4 ± 2.6%, p < 0.05). The lung wet to dry weight ratio was significantly increased in the PNP group (4.62 ± 0.31) compared to the CTR group (3.87 ± 0.22, p < 0.05). IV rhAPC administration tends to increase this parameter in  Pa -induced ALI (5.80 ± 0.66, p = 0.07). These findings were associated with a loss of inflammatory response compartmentalization measured by TNFα and IL-6 systemic levels. TAT complexes in BALF were increased in the A-PNP group (23.17 ± 2.89 ng/ml) compared to the CTR group (0.92 ± 0.17 ng/ml, p < 0.05) and the PNP group (11.06 ± 2.76 ng/ml, p < 0.05).    Conclusion  rhAPC reduces LLC following  Pa -induced ALI and may influence pulmonary edema formation. The early massive fibrin formation is probably beneficial in ALI limiting both the extent of injury and permeability disorders.

Intravenous administration of activated protein C in Pseudomonas-induced lung injury: impact on lung fluid balance and the inflammatory response