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Pulmonary changes in a mouse model of combined burn and smoke inhalation-induced injury

Departments of ¹Anesthesiology, ²Neuroscience and Cell Biology, and ³Pathology, University of Texas Medical Branch and Shriners Hospital for Children, Galveston, Texas; and ⁴Department of Anesthesiology and Intensive Care Unit, Oita University Faculty of Medicine, Oita, Japan

Submitted 27 February 2007 ; accepted in final form 10 April 2008

The morbidity and mortality of burn victims increase when burn injury is combined with smoke inhalation. The goal of the present study was to develop a murine model of burn and smoke inhalation injury to more precisely reveal the mechanistic aspects of these pathological changes. The burn injury mouse group received a 40% total body surface area third-degree burn alone, the smoke inhalation injury mouse group received two 30-s exposures of cotton smoke alone, and the combined burn and smoke inhalation injury mouse group received both the burn and the smoke inhalation injury. Animal survival was monitored for 120 h. Survival rates in the burn injury group, the smoke inhalation injury group, and the combined injury group were 70%, 60%, and 30%, respectively. Mice that received combined burn and smoke injury developed greater lung damage as evidenced by histological changes (septal thickening and interstitial edema) and higher lung water content. These mice also displayed more severely impaired pulmonary gas exchange [arterial PO₂ (Pa_O2)/inspired O₂ fraction (FI_O2) < 200]. Lung myeloperoxidase activity was significantly higher in burn and smoke-injured animals compared with the other three experimental groups. Plasma NO₂^–/NO₃^–, lung inducible nitric oxide synthase (iNOS) activity, and iNOS mRNA increased with injury; however, the burn and smoke injury group exhibited a higher response. Severity of burn and smoke inhalation injury was associated with more pronounced production of nitric oxide and accumulation of activated leukocytes in lung tissue. The murine model of burn and smoke inhalation injury allows us to better understand pathophysiological mechanisms underlying cardiopulmonary morbidity secondary to burn and smoke inhalation injury.

acute lung injury; inducible nitric oxide synthase; nitric oxide