[1]孙磊,陈晟,蔡颖,等.军用密闭舱室烟雾吸入致雄性大鼠心、肺、肝、肾损伤的观察[J].第三军医大学学报,2017,39(06):499-503.
 Sun Lei,Chen Sheng,Cai Ying,et al.Preliminary observation of heart, lung, liver and kidney injury in rats induced by smoke inhalation in military airtight cabins[J].J Third Mil Med Univ,2017,39(06):499-503.
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军用密闭舱室烟雾吸入致雄性大鼠心、肺、肝、肾损伤的观察(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
39卷
期数:
2017年第06期
页码:
499-503
栏目:
军事医学
出版日期:
2017-03-30

文章信息/Info

Title:
Preliminary observation of heart, lung, liver and kidney injury in rats induced by smoke inhalation in military airtight cabins
作者:
孙磊陈晟蔡颖崔志鸿刘文斌陶成玉刘晋祎曹佳
第三军医大学军事预防医学院毒理学研究所
Author(s):
Sun Lei Chen Sheng Cai Ying Cui Zhihong Liu Wenbin Tao Chengyu Liu Jinyi Cao Jia

Institute of Toxicology, College of Military Preventive Medicine, Third Military Medical University, Chongqing, 400038, China

关键词:
军用密闭舱室烟雾吸入系统毒性雄性大鼠
Keywords:
military airtight cabin  smoke inhalation systemic toxicity male rats
分类号:
R-332;R363.374;R644
文献标志码:
A
摘要:

目的      探讨军用密闭舱室非金属材料燃烧释放的有毒烟雾对雄性大鼠心、肺、肝、肾损伤的特点。方法     建立密闭舱室内动物烟雾吸入模型,将36只雄性SD大鼠按随机数字表法分为对照组及烟雾吸入后1、6、24、72 h和7 d组,对照组动物于染毒箱内自由呼吸新鲜空气10 min,染毒组动物于染毒箱内连续吸入烟雾10 min,观察烟雾吸入后动物的中毒症状、血压、心率、血气、血清生化等指标。结果     烟雾吸入后,动物立刻出现呼吸节律改变、呼吸困难等CO中毒表现;烟雾吸入后1 h大鼠心率显著下降(P<0.05),pCO2显著升高(P<0.05),pO2显著降低(P<0.05);烟雾吸入后1~72 h组动物谷丙转氨酶(ALT)均显著升高(P<0.05),其中6 h时达峰值(P<0.01);烟雾吸入后各组AST、LDH、α-HBDH、CK及CK-MB等心肌酶谱指标均持续升高,其中1 h组各指标与对照组比较差异均有统计学意义(P<0.05)。结论      密闭舱室火灾烟雾吸入首先对大鼠的肺脏造成原发性损伤,心、肝、肾产生继发性的功能损害,且上述功能损害主要发生在烟雾吸入后“24 h”窗口期内,其后由于机体代偿可逐渐恢复至正常。

Abstract:

Objective     To investigate the characteristics of rat heart, lung, liver and kidney injury induced by toxic smoke released from combustion of non-metal materials in military airtight cabins. Methods     On the basis of animal smoke inhalation model established in our laboratory, 36 male SD rats were divided randomly into control group and 5 inhalation groups (1, 6, 24 and 72 h, and 7 d after smoke exposure), and the clinical symptoms of poisoning, blood pressure, heart rate, blood gas, and serum biochemical indexes were observed after smoke inhalation. Results     After smoke inhalation, the symptoms of CO poisoning, such as respiratory rhythm change and breathing difficulties, were observed immediately. Compared with the control group, the heart rate was decreased in the rats exposed to the smoke, pCO2 increased, and pO2 declined significantly at 1 h after exposure (P<0.05). The level of alanine aminotransferase (ALT) was increased significantly in 1~72 h after exposure (P<0.05) and reached a peak at 6 h after exposure (P<0.01). The levels of AST, LDH, α-HBDH, CK and CK-MB were increased constantly in the rats after smoke inhalation, and all of the indexes above were elevated significantly in the group of 1 h post-exposure as compared with the control group (P<0.05). Conclusion     Smoke inhalation in military airtight cabins can cause primary injury to the lungs and secondary injury to the heart, liver and kidneys mainly within 24 h after exposure, and the body can gradually recover to the normal state because of compensation.

参考文献/References:

[1]CTIF. Center of Fire Statistics: World Fire Statistics, Report No 21[EB/OL]. [2016-05-23], http://www.ctif.org/sites/default/files/ctif_report21_world_fire_statistics_2016.pdf.
[2]李安, 柳海涛, 尹建华, 等. DNA鉴定在火灾事件中的应用[J]. 昆明医学院学报, 2007, 28: 59-61.
Li A, Liu H T, Yin J H, et al. The application of the DNA identification in fire accident[J]. Journal Kunming Medical College, 2007, 28: 59-61.
[3]Stefanidou M, Athanaselis S, Spiliopoulou C. Health impacts of fire smoke inhalation[J]. Inhal Toxicol, 2008, 20(8): 761-766. DOI:10.1080/08958370801975311
[4]杨宗城. 吸入性损伤研究进展[J]. 中华烧伤杂志, 2000, 16(3): 137-140.
Yang Z H. Research progress of inhalation burns [J]. Chinese Journal of Burns , 2000, 16(3): 137-140.
[5]Adetona O, Reinhardt T E, Domitrovich J, et al. Review of the health effects of wildland fire smoke on wildland fire-fighters and the public[J]. Inhal Toxicol, 2016, 28(3): 95-139. DOI:10.3109/08958378.2016.1145771
[6]Han Z H, Jiang Y I, Duan Y Y, et al. Protective effects of hydrogen sulfide inhalation on oxidative stress in rats with cotton smoke inhalation-induced lung injury[J]. Exp Ther Med, 2015, 10(1): 164-168. DOI:10.3892/etm.2015.2482
[7]Sun L, Zhao X, Li D, et al. A dynamic smoke generation and nose-only inhalation exposure system for rats: preliminary results from studies of selected transportation materials[J]. Inhal Toxicol, 2014, 26(14): 897-907. DOI:10.3109/08958378.2014.975874
[8]孙磊, 安辉, 郑有科, 等. 模拟密闭舱室烟雾吸入染毒装置的研制[J]. 第三军医大学学报, 2009, 31(4): 290-293.
Sun L, An H, Zheng Y K, et al. Development of a smoke inhalation unit simulating airtight cabin[J]. J Third Mil Med Univ, 2009, 31(4): 290-293.
[9]安辉, 孙磊, 周燕虹, 等. 密闭舱室内非金属材料燃烧释放有毒气体对大鼠肺组织通透性的影响[J]. 第三军医大学学报, 2009, 31(4): 294-296.
An H, Sun L, Zhou Y H, et al.Effect of poisonous gas produced from combustion of nonmetal materials on rat pulmonary microvascular permeability[J]. J Third Mil Med Univ, 2009, 31(04): 294-296.
[10]Antonio A C, Castro P S, Freire L O. Smoke inhalation injury during enclosedspace fires: an update[J]. J Bras Pneumol, 2013, 39(3): 373-381. DOI:10.1590/S1806-37132013000300016
[11]Ballard-Croft C, Sumpter L R, Broaddus R, et al. Ovine smoke/burn ARDS model: a new ventilator-controlled smoke delivery system[J]. J Surg Res, 2010, 164(1): e155-e162. DOI:10.1016/j.jss.2010.05.042
[12]Yilin Z, Yandong N, Faguang J. Role of angiotensin-converting enzyme (ACE) and ACE2 in a rat model of smoke inhalation induced acute respiratory distress syndrome[J]. Burns, 2015, 41(7): 1468-1477. DOI:10.1016/j.burns.2015.04.010
[13]Abali A E, Karakayali H, Ozdemir B H, et al. Destructive pulmonary effects of smoke inhalation and simultaneous alterations in circulating IL-6, TNF-α, and IFN-γ levels at different burn depths: an experimental study on rats[J]. J Burn Care Res, 2013, 34(3): 334-341. DOI:10.1097/BCR.0b013e3182644e9b
[14]Zhu F, Qiu X, Wang J, et al. A rat model of smoke inhalation injury[J]. Inhal Toxicol, 2012, 24(6): 356-364. DOI:10.3109/08958378.2012.673179
[15]Lee H M, Greeley G H, Englander E W. Transgenic overexpression of neuroglobin attenuates formation of smoke-inhalation-induced oxidative DNA damage, in vivo, in the mouse brain[J]. Free Radical Biology and Medicine, 2011, 51(12): 2281-2287. DOI:10.1016/j.freeradbiomed.2011.09.026
[16]Roderique J D, Josef C S, Feldman M J, et al. A modern literature review of carbon monoxide poisoning theories, therapies, and potential targets for therapy advancement[J]. Toxicology, 2015, 334: 45-58. DOI:10.1016/j.tox.2015.05.0041
[17]Hamahata A, Enkhbaatar P, Kraft E R, et al. γ-Tocopherol nebulization by a lipid aerosolization device improves pulmonary function in sheep with burn and smoke inhalation injury[J]. Free Radical Biology and Medicine, 2008, 45(4): 425-433. DOI:10.1016/j.freeradbiomed.2008.04.037
[18]Qiu X, Ji S, Wang J, et al. The therapeutic efficacy of Ulinastatin for rats with smoking inhalation injury[J]. Int Immunopharmacol, 2012, 14(3): 289-295. DOI:10.1016/j.intimp.2012.08.002
[19]Yamamoto Y, Sousse L E, Enkhbaatar P, et al. γ-tocopherol nebulization decreases oxidative stress, arginase activity, and collagen deposition after burn and smoke inhalation in the ovine model[J]. Shock, 2012, 38(6): 671-676. DOI:10.1097/SHK.0b013e3182758759
[20]Karapirli M, Kandemir E, Akyol S, et al. Forensic and clinical carbon monoxide (CO) poisonings in Turkey: A detailed analysis[J]. J Forensic Leg Med, 2013, 20(2): 95-101. DOI:10.1016/j.jflm.2012.04.031

相似文献/References:

[1]孙磊,安辉,郑有科,等.模拟密闭舱室烟雾吸入染毒装置的研制[J].第三军医大学学报,2009,31(04):290.
 SUN Lei,AN Hui,ZHENG You-ke,et al.Development of a smoke inhalation unit simulating airtight cabin[J].J Third Mil Med Univ,2009,31(06):290.
[2]安辉,孙磊,周燕虹,等.密闭舱室内非金属材料燃烧释放有毒气体对大鼠肺组织通透性的影响[J].第三军医大学学报,2009,31(04):294.
 AN Hui,SUN Lei,ZHOU Yan-hong,et al.Effect of poisonous gas produced from combustion of nonmetal materials on rat pulmonary microvascular permeability[J].J Third Mil Med Univ,2009,31(06):294.
[3]杨天德,杨宗城,黎鳌,等.烟雾吸入伤大鼠肺内部分磷脂酶A2变化特征与氟碳溶液部分液体通气影响的实验研究[J].第三军医大学学报,1997,19(01):0.[doi:10.16016/j.1000-5404.1997.01.011 ]

更新日期/Last Update: 2017-03-25