水下冲击波致比格犬肺和颅脑损伤特点
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摘要
目的研究水下冲击波对水下比格犬肺和颅脑的损伤程度。方法取标准比格犬18只,根据爆炸距离随机分为6组:对照组和5个实验组(距离爆源5 m、7 m、9 m、11 m、13 m组)。利用自制的水下爆炸装置对比格犬进行爆炸致伤,采用水下高速摄像观察爆炸致伤的动态过程。爆炸后6 h对比格犬行头颅和胸部计算机断层扫描(CT)平扫检查。爆炸后24 h取脑和肺标本,观察并记录颅脑和胸肺损伤的情况,对海马组织和肺组织进行H-E染色。采用免疫组织化学染色方法检测海马组织中炎性因子白细胞介素(IL)-6、IL-1β、IL-10、肿瘤坏死因子α(TNF-α)和转化生长因子β(TGF-β)的表达水平。结果高速摄影观察到爆炸对比格犬的毁伤包括冲击波和气泡脉动2个过程。实验组比格犬总死亡率为40.0%(6/15)。CT检查示实验组比格犬颅脑无大体损伤,肺部有胸腔积液、气胸等表现。H-E染色结果示实验组比格犬海马组织炎症细胞浸润,肺泡腔红细胞淤积。免疫组织化学染色结果示各实验组比格犬海马组织中IL-6、IL-1β、IL-10、TNF-α和TGF-β的表达水平与对照组相比均升高,差异均有统计学意义(P均<0.05)。结论脑、肺部等重要脏器受水下冲击波作用后会发生严重病变,是致动物死亡的主要原因;进一步探索水下冲击波致颅脑损伤的机制对于水下冲击伤的防护有重要意义。
Objective To explore underwater shock wave-induced injuries of the lung and brain in canines.Methods Eighteen Beagle dogs were randomly divided into six groups according to the distances to the explosion source:control group and 5 experimental groups(5 m, 7 m, 9 m, 11 m and 13 m groups). The animals were exposed to underwater shock wave via a self-designed underwater explosive instrument. The dynamic explosive process was recorded by the underwater highspeed camera. Computed tomography(CT) scans of brain and chest were performed 6 h after injury. Pathological examination and H-E staining for hippocampus and lung were conducted 24 h after injury. The expression levels of interleukin(IL)-6,IL-1β, IL-10, tumor necrosis factor α(TNF-α) and transforming growth factor β(TGF-β) in the hippocampus were measured by immunohistochemical staining. Results The underwater high-speed camera showed that the injury process included blast wave and bubble pulsation. The total mortality of the animals was 40.0%(6/15) in the experimental groups. CT examination revealed no major alterations in the brain of the animals, while there were pleural effusion and pneumothorax in the chest of animals in the experimental groups. H-E staining showed inflammatory cells infiltration in the hippocampal tissue and erythrocyte deposition in the alveoli of animals in the experimental groups. The expression levels of IL-6, IL-1β, IL-10, TNF-α, and TGF-β in the hippocampus of animals in the experimental groups were significantly elevated compared with those in control group(all P<0.05).Conclusion Brain and chest are damaged significantly after underwater explosion, which may be the main causes for the death of animals. It is important to elucidate the underlying mechanisms of brain injury caused by underwater explosive wave for the protection of underwater blast injuries.
Objective To explore underwater shock wave-induced injuries of the lung and brain in canines.Methods Eighteen Beagle dogs were randomly divided into six groups according to the distances to the explosion source:control group and 5 experimental groups(5 m, 7 m, 9 m, 11 m and 13 m groups). The animals were exposed to underwater shock wave via a self-designed underwater explosive instrument. The dynamic explosive process was recorded by the underwater highspeed camera. Computed tomography(CT) scans of brain and chest were performed 6 h after injury. Pathological examination and H-E staining for hippocampus and lung were conducted 24 h after injury. The expression levels of interleukin(IL)-6,IL-1β, IL-10, tumor necrosis factor α(TNF-α) and transforming growth factor β(TGF-β) in the hippocampus were measured by immunohistochemical staining. Results The underwater high-speed camera showed that the injury process included blast wave and bubble pulsation. The total mortality of the animals was 40.0%(6/15) in the experimental groups. CT examination revealed no major alterations in the brain of the animals, while there were pleural effusion and pneumothorax in the chest of animals in the experimental groups. H-E staining showed inflammatory cells infiltration in the hippocampal tissue and erythrocyte deposition in the alveoli of animals in the experimental groups. The expression levels of IL-6, IL-1β, IL-10, TNF-α, and TGF-β in the hippocampus of animals in the experimental groups were significantly elevated compared with those in control group(all P<0.05).Conclusion Brain and chest are damaged significantly after underwater explosion, which may be the main causes for the death of animals. It is important to elucidate the underlying mechanisms of brain injury caused by underwater explosive wave for the protection of underwater blast injuries.
引文
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[10]黄代新,张林,吴梅筠,陈于波,吴家.大鼠液压冲击脑损伤后bFGF及其受体FGFR1的表达[J].法医学杂志,2004,20:65-67.
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[12]WINTER C D,PRINGLE A K,CLOUGH G F,CHURCH M K.Raised parenchymal interleukin-6 levels correlate with improved outcome after traumatic brain injury[J].Brain,2004,127(Pt 2):315-320.
[13]LIAO Y,LIU P,GUO F,ZHANG Z Y,ZHANG Z.Oxidative burst of circulating neutrophils following traumatic brain injury in human[J/OL].PLoS One,2013,8:e68963.doi:10.1371/journal.pone.0068963.
[14]TOKLU H Z,YANG Z,OKTAY S,SAKARYA Y,KIRICHENKO N,MATHENY M K,et al.Overpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum[J].Behav Brain Res,2018,340:14-22.
[15]KOCHANEK P M,DIXON C E,SHELLINGTON D K,SHIN S S,BAYIR H,JACKSON E K,et al.Screening of biochemical and molecular mechanisms of secondary injury and repair in the brain after experimental blastinduced traumatic brain injury in rats[J].J Neurotrauma,2013,30:920-937.
[2]杨志焕,朱佩芳,蒋建新,尹志勇,周继红,李晓炎,等.水下冲击波的生物效应[J].爆炸与冲击,2003,23:134-139.
[3]张丹枫,张孝凤,李雅,侯立军,王君玉,陈吉钢,等.一种动物水下试验装置:CN206315158U[P].2017-07-11.
[4]王峰.特殊环境冲击伤的伤情特点和治疗研究[D].重庆:第三军医大学,2008.
[5]张波,刘大维,蒋建新,杨志焕,朱佩芳,王正国.犬水下冲击伤后主要脏器的病理学变化[J].第三军医大学学报,2003,25:938-940.
[6]张丹枫,陈吉钢,王春晖,李振兴,侯立军.水下爆炸损伤生物效应研究现状及展望[J].第二军医大学学报,2016,37:1283-1286.ZHANG D F,CHEN J G,WANG C H,LI Z X,HOU L J.Biological effect of underwater explosion injury:research progress and prospective[J].Acad J Sec Mil Med Univ,2016,37:1283-1286.
[7]MCKEE C A,LUKENS J R.Emerging roles for the immune system in traumatic brain injury[J/OL].Front Immunol,2016,7:556.doi:10.3389/fimmu.2016.00556.
[8]GARCIA J M,STILLINGS S A,LECLERC J L,PHILLIPS H,EDWARDS N J,ROBICSEK S A,et al.Role of interleukin-10 in acute brain injuries[J/OL].Front Neurol,2017,8:244.doi:10.3389/fneur.2017.00244.
[9]ZEILER F A,THELIN E P,CZOSNYKA M,HUTCHINSON P J,MENON D K,HELMY A.Cerebrospinal fluid and microdialysis cytokines in severe traumatic brain injury:a scoping systematic review[J/OL].Front Neurol,2017,8:331.doi:10.3389/fneur.2017.00331.
[10]黄代新,张林,吴梅筠,陈于波,吴家.大鼠液压冲击脑损伤后bFGF及其受体FGFR1的表达[J].法医学杂志,2004,20:65-67.
[11]KUMAR R G,BOLES J A,WAGNER A K.Chronic inflammation after severe traumatic brain injury:characterization and associations with outcome at 6 and12 months postinjury[J].J Head Trauma Rehabil,2015,30:369-381.
[12]WINTER C D,PRINGLE A K,CLOUGH G F,CHURCH M K.Raised parenchymal interleukin-6 levels correlate with improved outcome after traumatic brain injury[J].Brain,2004,127(Pt 2):315-320.
[13]LIAO Y,LIU P,GUO F,ZHANG Z Y,ZHANG Z.Oxidative burst of circulating neutrophils following traumatic brain injury in human[J/OL].PLoS One,2013,8:e68963.doi:10.1371/journal.pone.0068963.
[14]TOKLU H Z,YANG Z,OKTAY S,SAKARYA Y,KIRICHENKO N,MATHENY M K,et al.Overpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum[J].Behav Brain Res,2018,340:14-22.
[15]KOCHANEK P M,DIXON C E,SHELLINGTON D K,SHIN S S,BAYIR H,JACKSON E K,et al.Screening of biochemical and molecular mechanisms of secondary injury and repair in the brain after experimental blastinduced traumatic brain injury in rats[J].J Neurotrauma,2013,30:920-937.