title: Cardiopulmonary, histological, and inflammatory alterations after lung contusion in a novel mouse model of blunt chest trauma.
abstract: Severe blunt chest trauma remains an important injury with high morbidity and mortality. However, the associated immunological alterations are poorly understood. Existing big animal models require large-scale settings, are often too expensive, and research products for immunological studies are limited. In this study we aimed to establish a new model of blunt, isolated and bilateral chest trauma in mice and to characterize its effects on physiological and inflammatory variables. Male C3H/HeN mice (n = 9-10/group) were anesthetized and a femoral artery was catheterized. The animals were subjected to trauma or sham procedure and monitored for 180 min. Blunt chest trauma was induced by a blast wave focused on the thorax. Trauma intensity was optimized by varying the exposure distance. Blood pressure, heart rate, respiratory rate, arterial blood gases and plasma cytokine levels were measured. Macroscopic and microscopic examinations were performed. In addition, outcome was evaluated in a 10-day survival study. Chest trauma caused a drop (P < 0.05) in blood pressure and heart rate, which partly recovered. Blood gases revealed hypoxemia and hypercarbia (P < 0.05) 180 min after trauma. There was marked damage to the lungs but none to abdominal organs. Histologically, the characteristic signs of a bilateral lung contusion with alveolar and intrabronchial hemorrhage were found. Plasma interleukin-6 and tumor necrosis factor alpha were considerably increased after 180 min. Blunt chest trauma resulted in an early mortality of 10% without subsequent death. On the basis of these findings, this novel mouse model of blunt chest trauma appears suitable for detailed studies on immunological effects of lung contusion.
authors.affiliation: Department of Trauma, Hand, and Reconstructive Surgery, University of Ulm, 89075 Ulm, Germany.
authors.forename: Markus W
authors.initials: MW
authors.lastname: Knöferl
authors.forename: Ulrich C
authors.initials: UC
authors.lastname: Liener
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Seitz
authors.forename: Mario
authors.initials: M
authors.lastname: Perl
authors.forename: Uwe B
authors.initials: UB
authors.lastname: Brückner
authors.forename: Lothar
authors.initials: L
authors.lastname: Kinzl
authors.forename: Florian
authors.initials: F
authors.lastname: Gebhard
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003288:Contusions / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D016207:Cytokines / Q000097:blood*; D004195:Disease Models, Animal; D006339:Heart Rate; D007249:Inflammation / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D008171:Lung Diseases / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D015656:Respiratory Mechanics / Q000502:physiology*; D016019:Survival Analysis; D013898:Thoracic Injuries / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors; D014949:Wounds, Nonpenetrating / Q000473:pathology / Q000503:physiopathology*
chemical_list: D016207:Cytokines