title: Fibrinolytic activity in bronchoalveolar lavage of baboons with diffuse alveolar damage: trends in two forms of lung injury.
abstract: METHODS
  Alveolar fibrin deposition is prominent in diffuse alveolar damage, the morphologic hallmark of the adult respiratory distress syndrome. To determine if a persistent abnormality of fibrin clearance occurs in the alveolar compartment during evolving diffuse alveolar damage, we characterized abnormalities of fibrin turnover in serial bronchoalveolar lavage specimens from two baboon models: a) diffuse alveolar damage induced by 80% oxygen and bronchoscopic seeding of Pseudomonas aeruginosa; and b) a more fulminant form of diffuse alveolar damage induced by bronchoscopic seeding of Pseudomonas and the infusion of oleic acid.
  
  
  RESULTS
  Lavage procoagulant activity, due mainly to tissue factor associated with Factor VII, was increased and exceeded regulation by extrinsic pathway inhibitor in both models. Fibrinolytic activity was transiently diminished in baboons with evolving diffuse alveolar damage induced by oleic acid/Pseudomonas, but was preserved after 80% oxygen/Pseudomonas. Concentrations of plasminogen activator inhibitor-2 did not increase in lavage specimens obtained during evolving diffuse alveolar damage. Concentrations of alpha 2 antiplasmin and plasminogen activator inhibitor-1 tended to be higher in the lavage of oleic acid/Pseudomonas baboons with low fibrinolytic activity. Immunohistochemical analyses showed that tissue factor was distributed along the alveolar surface of controls and baboons with diffuse alveolar damage. Alveolar fibrin deposition was increased, by morphometric analyses, in both models.
  
  
  CONCLUSIONS
  These data indicate that while increased procoagulant activity is characteristic of evolving diffuse alveolar damage and favors alveolar fibrin deposition, fibrinolytic activity may be transiently diminished or remain intact during evolving diffuse alveolar damage in baboons.
authors.affiliation: Department of Medicine, University of Texas Health Center, Tyler 75710.
authors.forename: S
authors.initials: S
authors.lastname: Idell
authors.forename: K K
authors.initials: KK
authors.lastname: James
authors.forename: J J
authors.initials: JJ
authors.lastname: Coalson
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry* / Q000378:metabolism; D001999:Bronchoscopy; D004195:Disease Models, Animal; D005069:Evaluation Studies as Topic; D005337:Fibrin / Q000032:analysis / Q000378:metabolism*; D005342:Fibrinolysis; D007150:Immunohistochemistry; D008657:Metabolic Clearance Rate; D019301:Oleic Acid; D009829:Oleic Acids; D010100:Oxygen / Q000009:adverse effects; D010215:Papio; D010958:Plasminogen / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D017396:Plasminogen Activator Inhibitor 2 / Q000032:analysis; D011550:Pseudomonas aeruginosa / Q000254:growth & development; D011658:Pulmonary Fibrosis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D012128:Respiratory Distress Syndrome / Q000378:metabolism / Q000473:pathology; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014568:Urokinase-Type Plasminogen Activator / Q000032:analysis; D000979:alpha-2-Antiplasmin / Q000032:analysis
chemical_list: D009829:Oleic Acids; D017395:Plasminogen Activator Inhibitor 1; D017396:Plasminogen Activator Inhibitor 2; D000979:alpha-2-Antiplasmin; D019301:Oleic Acid; D005337:Fibrin; D010958:Plasminogen; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator; D010100:Oxygen