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The study on the longer time course of seawater aspiration-induced acute lung injury and stress response |
Yuan Jia-jia, Zhang Xiao-tong, Bao Yun-ting, Xu Zheng-qing, Shu Yuan-zhao, Wang Zi-wei, Du Bin, Pang Qing-feng |
Department of Pathophysiology, Medical School of Jiangnan University, Wuxi 214122, China |
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Abstract Objective: To observe the morphological and biochemical index of seawater aspiration-induced acute lung injury from 15 min to 3 d after drowning. Methods: A total of 84 male mice were assigned to 10 groups including normal group(10), non-survival group(22) and near-drowning 15 min(10), 30 min(6),1 h(6), 3 h(6), 6 h(6), 12 h(6), 24 h(6), 72 h(6). Lung wet-to-dry weight ratio, blood gas and biochemical analysis were examined in the normal group, near, drowning 15 min group, and non-survival group. The computed tomography images were obtained using 64 mA 120 kV with a voxel of 1.0 mm. The activity of superoxide dismutase, the content of methane dicarboxylic aldehyde, the content and activity of heme oxygease-1, and the content of aquaporin-1 in the lung tissue were determined. The pulmonary histological changes were observed under light microscope. Results: Compared with normal group, the lung injury in near- drowning 15 min, 30 min, 1 h, 3 h, 6 h groups was more serious, especially in 1 h group. In 1 h group, the level of methane dicarboxylic aldehyde is highest while superoxide dismutase activity was lowest. The expression and enzymatic activity of heme oxygease-1 significantly increased and were sustainable for 3 d. Meanwhile, aquaporin -1 expression increased at peak in 6 h group. Conclusion: The seawater aspiration- induced lung injury can self-repair partly dependent on heme oxygease-1 and aquaporin-1.
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Received: 09 May 2017
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Corresponding Authors:
Pang Qing-feng, E-mail: qfpang@jiangnan.edu.cn
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[1]Bierens JJ, Lunetta P, Tipton M, et al. Physiology of drowning: a review [J]. Physiology(Bethesda), 2016, 31(2): 147-166.
[2]Leavy JE, Crawford G, Leaversuch F, et al. A Review of Drowning Prevention Interventions for Children and Young People in High, Low and Middle Income Countries [J]. J Community Health, 2016, 41(2): 424-441.
[3]Ji MH, Tong JH, Tan YH, et al. Erythropoietin Pretreatment Attenuates Seawater Aspiration-Induced Acute Lung Injury in Rats [J]. Inflammation, 2016, 39(1): 447-456.
[4]Liu Z, Zhang B, Wang XB, et al. Hypertonicity contributes to seawater aspiration-induced lung injury: Role of hypoxia-inducible factor 1α [J]. Exp Lung Res, 2015, 41(6): 301-315.
[5]Liu QP, Zhou DX, Sun L, et al. Bone marrow mesenchymal stem cells ameliorates seawater-exposure-induced acute lung injury by inhibiting autophagy in lung tissue [J]. Patholog Res Int, 2014, 2014:104 962.
[6]孙荣距, 赵晓东, 黎檀实. 溺水急救过程中的几点问题思考[J]. 中国急救医学, 2015, 35(8): 762-764.
[7]刘东虎. 心肺复苏培训与溺水患者抢救成功率相关研究[J]. 中国社区医师(医学专业), 2013, 13(3): 193-194.
[8]姚慧文, 陈键腾, 赵莺柳. 无创性双水平正压通气抢救淹溺后肺水肿的疗效观察[J]. 中国医药导报, 2009, 6(9): 37-38.
[9]刘新军, 李会文, 王玉红, 等. 淹溺患者院外心肺复苏分析[J]. 中国药物经济学, 2014, 10: 259-260.
[10]Gaggar A, Patel RP. There is blood in the water: hemolysis, hemoglobin, and heme in acute lung injury[J]. Am J Physiol Lung Cell Mol Physiol, 2016, 311(4): L714-L718.
[11]Pang QF, Ji Y, Bermúdez-Humarán LG, et al. Protective effects of a heme oxygenase-1-secreting Lactococcus lactis on mucosal injury induced by hemorrhagic shock in rats [J]. J Surg Res, 2009, 153(1): 39-45.
[12]Yu J, Wang Y, Li Z, et al. Effect of Heme Oxygenase-1 on Mitofusin-1 protein in LPS-induced ALI/ARDS in rats [J]. Sci Rep, 2016, 6: 36 530.
[13]Dolinay T, Choi AM, Ryter SW. Heme Oxygenase-1/CO as protective mediators in cigarette smoke-induced lung cell injury and chronic obstructive pulmonary disease [J]. Curr Pharm Biotechnol, 2012, 13(6): 769-776.
[14]An L, Liu CT, Yu MJ, et al. Heme oxygenase-1 system, inflammation and ventilator-induced lung injury [J]. Eur J Pharmacol, 2012, 677(1-3):1-4.
[15]Pang QF, Zhou QM, Zeng S, et al. Protective effect of hemeoxygenase-1 on lung injury induced by erythrocyte instillation in rats [J]. Chin Med J(Engl), 2008, 121(17): 1688-1692.
[16]Zelenina M, Zlelnin S, Aperia A. Water channels(aquaporins)and their role for postnatal adaptation [J]. Pediatr Res, 2005, 7(5 Pt 2): 47R-53R.
[17]Borok Z, Lubman RL, Danto SI, et al. Keratinocyte growth factor modulates alveolar epithelial cell phenotype in vitro: expression of aquaporin 5 [J]. Am J Respir Cell Mol Biol, 1998, 18(4): 554-561.
[18]范启新. 17β-雌二醇在海水淹溺性肺水肿中的作用及其机制[D]. 第四军医大学, 2010.
[19]胡华子, 陈阳, 廖志铜, 等. 溺死大鼠肺组织水通道蛋白1的表达[J]. 法医学杂志, 2004, 20(1): 13-14.
[20]赵兵,姚士强,郝小惠. 溺死大鼠肺组织AQP-1、AQP-4的表达[J]. 法医学杂志, 2016, 32(5): 321-325. |
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