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| Establishment and evaluation of animal model of smoke inhalation injury |
| Xiao Pei-xin, Sun Shu-li, Wang Jing, Li He-lin, Ding Hui, Bai Song, Liu Zi-quan, Cao Juan, Liu Jin-yang, Wang Xue, Lv Qi, Fan Hao-jun |
| Postgraduate Training Base in Affiliated Hospital of Logistics University of People′s Armed Police Force,Jinzhou Medical University, Tianjin 300162, China |
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Abstract Objective To establish rats model of smoke inhalation injury, and explore the changes of pathophysiology and inflammatory factors in rats after injury. Methods 42 male Wistar rats were randomly divided into 7 groups: normal control group (n=6)and smoke inhalation injury 6 groups (n=36). The rats were sampled after being injured 1, 2, 3, 7, 14 and 28 days (n=6), and the pathological changes of the lung tissue were observed by HE staining. The degree of pulmonary edema was evaluated by measuring wet and dry weight ratio (W/D ratio)of lung tissue. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in plasma and bronchoalveolar lavage fluid were measured by enzyme-linked immuno sorbent assay (ELISA). Results The histopathology of lung tissue showed that the first 3 days after the injury was in the acute phase. The main change was airway lesion, with the ciliated structure of airway epithelial cells damaged, airway local secretions increased, the alveolar stroma thickening, alveolar rupture and fusion; At 7 days after the injury,the histopathological changes mainly included local pulmonary interstitial lesions, alveolar fusion, occasional inflammatory cell infiltration; At 28 days post-injury, large lamellar interstitial lesions were founded, which indicated local lung fibrosis. The wet and dry weight ratios of lung tissue in 1 day and 2 days injury groups were higher than that in normal controls (P=0.001,P=0.014). And, the W/D ratios of lung tissue in 7 days, 14 days and 28 days was significantly lower than those in 1 day group (P=0.018,P=0.024,P=0.014). Compared with the normal control group, plasma IL-6 did not change significantly after injury. IL-6 in alveolar lavage fluid did not change significantly and the content of IL-6 in 28 days group was slightly lower (P＜0.05). The level of TNF-α in plasma was significantly increased after 1 day of injury, and the content of TNF-α in 28 days group was significantly lower than that in normal control group (P<0.05). The content of TNF-α in alveolar lavage fluid was significantly increased after injury, and there were two peaks at 2 and 14 days after injury (P＜0.05). Conclusion The changes of pathologic damage and inflammatory factors after smoke inhalation showed some regularity. Our study provides experimental basis and strategy for elucidating the pathogenesis and treatment of smoke inhalation injury.
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Corresponding Authors:
Fan Hao-jun, E-mail:fanhaojun999@126.com
Lv Qi, E-mail:lvqi68@163.com
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| ［1］Rehberg S, Maybauer MO, Enkhbaatar P, et al. Pathophysiology, management and treatment of smoke inhalation injury［J］. Expert Rev Respir Med, 2009, 3(3):283-297.
［2］David P, Dunsford D, Lu J, et al. Animal models of smoke inhalation induced injuries［J］. Front Biosci(Landmark Ed), 2009, 14:4618-4630.
［3］Murakami K, Traber DL. Pathophysiological basis of smoke inhalation injury［J］. News PhysiolSci, 2003, 18:125-129.
［4］Kimmel EC, Still KR.Acute lung injury, acute respiratory distress syndrome and inhalationinjury: an overview［J］. Drug Chem Toxicol, 1999, 22, (1): 91-128.
［5］Demling RH. Smoke inhalation lung injury: an update［J］. Eplasty, 2008, 8:e27.
［6］de Oliveira HG, Guerra VA, Knorst MM. Fire-Related Inhalation Injury［J］. NEngl J Med, 2016, 375(19):1903-1904.
［7］Lange M, Hamahata A, Traber DL, et al. A murine model of sepsis following smoke inhalation injury［J］. Biochem Biophys Res Commun, 2010, 391(3):1555-1560.
［8］Zhu F, Qiu X, Wang J, et al. A rat model of smoke inhalation injury［J］. Inhal Toxicol, 2012, 24(6):356-364.
［9］Enkhbaatar P, Traber DL. Pathophysiology of acute lung injury in combined burn and smoke inhalation injury［J］. Clin Sci(Lond), 2004, 107(2):137-143.
［10］da Cunha AA, Nunes FB, Lunardelli A, et al. Treatment with N-methyl-D-aspartate receptor antagonist (MK-801)protects against oxidative stress in lipopolysaccharide-induced acute lung injury in the rat［J］. Int Immunopharmacol, 2011, 11(6):706-711.
［11］Kawamura T, Huang CS, Tochigi N, et al. Inhaled hydrogen gas therapy for prevention of lung transplant-induced ischemia/reperfusion injury in rats［J］. Transplantation, 2010, 90(12):1344-1351.
［12］Song M, Lv Q, Zhang X, et al. Dynamic Tracking Human Mesenchymal Stem Cells Tropism following Smoke Inhalation Injury in NOD/SCID Mice［J］. Stem Cells Int, 2016, 2016:1 691 856.
［13］ToonMH, MaybauerMO, Greenwood JE, et al. Management of acute smoke inhalation injury［J］. Crit Care Resusc, 2010, 12(1):53-61.
［14］Maybauer MO, Rehberg S, Traber DL, et al. Pathophysiology of acute lung injury in severe burn and smoke inhalation injury［J］. Anaesthesist, 2009, 58(8): 805-812.
［15］Enkhbaatar P, Pruitt BA Jr, Suman O,et al. Pathophysiology, research challenges, and clinical management of smoke inhalation injury［J］. Lancet, 2016, 388(10052):1437-1446.
［16］Finnerty CC, Herndon DN, Przkora R, et al. Cytokine expression profle over time in severely burned pediatric patients［J］. Shock, 2006, 26(1):13-19.
［17］Davis CS, Janus SE, Mosier MJ, et al. Inhalation injury severity and systemic immune perturbations in burned adults［J］. Ann Surg, 2013, 257(6):1137-1146.
［18］de Carvalho FO, Felipe FA, de Melo Costa AC, et al. Inflammatory Mediators and Oxidative Stress in Animals Subjected to Smoke Inhalation: A Systematic Review［J］. Lung, 2016, 194(4):487-499.
［19］Stromps JP, Fuchs P, Demir E, et al. Intraalveolar TNF-alpha in combined burn and inhalation injury compared with intraalveolar interleukin-6［J］. J Burn Care Res, 2015, 36(2): e55-61.
［20］Zhang F, Li MY, Lan YT, et al. Imbalance of Th17/Tregs in rats with smoke inhalation-induced acute lung injury［J］. Sci Rep, 2016, 6: 21 348.
［21］Redente EF, Keith RC, Janssen W, et al. Tumor necrosis factor-α accelerates the resolution of established pulmonary fibrosis in mice by targeting profibrotic lung macrophages［J］. Am J Respir Cell Mol Biol, 2014, 50(4):825-837.
［22］Kobayashi T, Tanaka K, Fujita T, et al. Bidirectional role of IL-6 signal in pathogenesis of lung fibrosis［J］. Respir Res, 2015, 16:99. |
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