Recombinant human activated protein C inhibits local and systemic activation of coagulation without influencing inflammation during Pseudomonas aeruginosa pneumonia in rats

Crit Care Med. 2007 May;35(5):1362-8. doi: 10.1097/01.CCM.0000261888.32654.6D.

Abstract

Objective: Alveolar fibrin deposition is a hallmark of pneumonia. It has been proposed that recombinant human activated protein C exerts lung-protective effects via anticoagulant and anti-inflammatory pathways. We investigated the role of the protein C system in pneumonia caused by Pseudomonas aeruginosa, the organism that is predominantly involved in ventilator-associated pneumonia.

Design: An observational clinical study and a controlled, in vivo laboratory study.

Setting: Multidisciplinary intensive care unit and a research laboratory of a university hospital.

Patients and subjects: Patients with unilateral ventilator-associated pneumonia and male Sprague-Dawley rats.

Interventions: Bilateral bronchoalveolar lavage was performed in five patients with unilateral ventilator-associated pneumonia. A total of 62 rats were challenged with intratracheal P. aeruginosa (10 colony-forming units), inducing pneumonia. Rats were randomized to treatment with normal saline, recombinant human activated protein C, heparin, or recombinant tissue plasminogen activator.

Measurements and main results: Patients with pneumonia demonstrated suppressed levels of protein C and activated protein C in bronchoalveolar lavage fluid obtained from the infected site compared with the contralateral uninfected site. Intravenous administration of recombinant human activated protein C in rats with P. aeruginosa pneumonia limited bronchoalveolar generation of thrombin-antithrombin complexes, largely preserving local antithrombin activity. However, recombinant human activated protein C did not have effects on neutrophil influx and activity, expression of pulmonary cytokines, or bacterial clearance.

Conclusions: In patients with ventilator-associated pneumonia, the pulmonary protein C pathway is impaired at the site of infection, and local anticoagulant activity may be insufficient. Recombinant human activated protein C prevents procoagulant changes in the lung; however, it does not seem to alter the pulmonary host defense against P. aeruginosa pneumonia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Infective Agents / administration & dosage*
  • Antithrombins / metabolism
  • Blood Coagulation / drug effects*
  • Bronchoalveolar Lavage Fluid / chemistry
  • Fibrinolytic Agents / administration & dosage*
  • Heparin / administration & dosage
  • Humans
  • Inflammation / drug therapy
  • Inflammation / metabolism*
  • Male
  • Neutrophils / metabolism
  • Pneumonia, Ventilator-Associated / drug therapy
  • Pneumonia, Ventilator-Associated / metabolism*
  • Protein C / administration & dosage*
  • Protein C / metabolism
  • Pseudomonas Infections / drug therapy
  • Pseudomonas Infections / metabolism*
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Recombinant Proteins / administration & dosage
  • Tenecteplase
  • Thrombin / metabolism
  • Thrombomodulin / metabolism
  • Tissue Plasminogen Activator / administration & dosage

Substances

  • Anti-Infective Agents
  • Antithrombins
  • Fibrinolytic Agents
  • Protein C
  • Recombinant Proteins
  • Thrombomodulin
  • Heparin
  • Thrombin
  • Tissue Plasminogen Activator
  • drotrecogin alfa activated
  • Tenecteplase