title: Inflammatory alterations in a novel combination model of blunt chest trauma and hemorrhagic shock.
abstract: BACKGROUND
  Chest trauma frequently occurs in severely injured patients and is often associated with hemorrhagic shock. Immune dysfunction contributes to the adverse outcome of multiple injuries. The aims of this study were to establish a combined model of lung contusion and hemorrhage and to evaluate the cardiopulmonary and immunologic response.
  
  
  METHODS
  Male mice were subjected to sham procedure, chest trauma, hemorrhage (35 mm Hg±5 mm Hg, 60 minutes), or the combination. Respiratory rate, heart rate, and blood pressure were monitored. Plasma, Kupffer cells, blood monocytes, splenocytes, and splenic macrophages were isolated after 20 hours. Tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, 10, 12, 18, and macrophage inflammatory protein-2 levels in plasma and culture supernatants were determined.
  
  
  RESULTS
  Heart rate and blood pressure dropped in all groups, and after chest trauma and the double hit, these values remained reduced until the end of observation. Blood pressure was lower after the double hit than after the single hits. Plasma and Kupffer cell TNF-α concentrations were increased after lung contusion but not further enhanced by subsequent hemorrhage. Peripheral blood mononuclear cell (PBMC) TNF-α and IL-6 release were suppressed after the combined insult. IL-18 concentrations were increased in PBMC supernatants after chest trauma and in splenic macrophage supernatants of all groups.
  
  
  CONCLUSIONS
  Although physiologic readouts were selectively altered in response to the single or double hits, the combination did not uniformly augment the changes in inflammation. Our results suggest that the leading insult regarding the immunologic response is lung contusion, supporting the concept that lung contusion represents an important prognostic factor in multiple injuries.
authors.affiliation: Department of Trauma Surgery, Hand, Plastic and Reconstructive Surgery and Division of Surgical Research, University of Ulm, Ulm, Germany.
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Seitz
authors.forename: Mario
authors.initials: M
authors.lastname: Perl
authors.forename: Ulrich C
authors.initials: UC
authors.lastname: Liener
authors.forename: Björn
authors.initials: B
authors.lastname: Tauchmann
authors.forename: Sonja T
authors.initials: ST
authors.lastname: Braumüller
authors.forename: Uwe B
authors.initials: UB
authors.lastname: Brückner
authors.forename: Florian
authors.initials: F
authors.lastname: Gebhard
authors.forename: Markus W
authors.initials: MW
authors.lastname: Knöferl
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D054426:Chemokine CXCL2 / Q000097:blood; D004195:Disease Models, Animal; D006339:Heart Rate / Q000502:physiology; D007378:Interleukins / Q000097:blood; D007958:Leukocyte Count; D008264:Macrophages / Q000502:physiology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D012771:Shock, Hemorrhagic / Q000150:complications* / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D013154:Spleen / Q000503:physiopathology; D013898:Thoracic Injuries / Q000150:complications* / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014949:Wounds, Nonpenetrating / Q000150:complications* / Q000276:immunology / Q000473:pathology / Q000503:physiopathology
chemical_list: D054426:Chemokine CXCL2; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha