title: Physiologic and biologic characteristics of three experimental models of acute lung injury in rats.
abstract: BACKGROUND
  Strategies to attenuate ventilator-associated lung injury have been tested in various experimental methods of acute lung injury (ALI). Conclusions are often drawn from physiologic and biologic effects, but the influence of the model on these results is not known. Our aim in this study was to characterize frequently used models of experimental ALI.
  
  
  METHODS
  Twenty Sprague Dawley rats were anesthetized and their lungs mechanically ventilated for 5 hours. Three models of ALI (surfactant washout, acid aspiration, and high tidal volume ventilation) were investigated with regard to hemodynamics, respiratory mechanics, gas exchange, lung pathology, and inflammatory reactions. Animals without ALI served as controls.
  
  
  RESULTS
  Five animals in each group were analyzed. Dynamic compliance and Pao(2)/fraction of inspired oxygen ratio decreased by at least 50% in all groups after 1 hour. Whereas compliance remained decreased in all models, oxygenation returned to baseline values in the lavage group after 5 hours. Diffuse alveolar damage was worse in the high tidal volume model and was not different between the control and lavage animals. Interleukin-6 was increased in bronchoalveolar lavage fluid in the aspiration and high tidal volume models.
  
  
  CONCLUSIONS
  Although comparable physiologic effects meeting acute respiratory distress syndrome criteria were achieved in all models, the biologic responses varied among lung injury models. The acid aspiration model created both respiratory and inflammatory responses typically seen in ALI; these data suggest that it may be the most clinically applicable model to study the intermediate-term effects of ventilator-associated lung injury in rats.
authors.affiliation: Department of Anesthesiology and Critical Care, Dalhousie University Halifax, QEII Health Sciences Center, 1276 South Park St., 10 West Victoria, Halifax, NS, B3H 2Y9, Canada. mail@d-henzler.de
authors.forename: Dietrich
authors.initials: D
authors.lastname: Henzler
authors.forename: Nadine
authors.initials: N
authors.lastname: Hochhausen
authors.forename: Raymond
authors.initials: R
authors.lastname: Chankalal
authors.forename: Zhaolin
authors.initials: Z
authors.lastname: Xu
authors.forename: Sara C
authors.initials: SC
authors.lastname: Whynot
authors.forename: Arthur S
authors.initials: AS
authors.lastname: Slutsky
authors.forename: Haibo
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D004195:Disease Models, Animal; D006439:Hemodynamics; D006470:Hemorrhage / Q000209:etiology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008168:Lung / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D008170:Lung Compliance; D008297:Male; D001261:Pulmonary Atelectasis / Q000209:etiology / Q000503:physiopathology; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology; D011659:Pulmonary Gas Exchange; D051381:Rats; D017207:Rats, Sprague-Dawley; D015656:Respiratory Mechanics; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation; D055397:Ventilator-Induced Lung Injury / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D016753:Interleukin-10