本文選題：艙室 + 爆炸傷��； 參考：《第三軍醫(yī)大學(xué)》2011年碩士論文

【摘要】：伊拉克戰(zhàn)爭、阿富汗戰(zhàn)爭中,以美國為主的多國部隊(duì)作戰(zhàn)人員主要在裝甲車輛等戰(zhàn)斗艙室內(nèi)作戰(zhàn),穿甲彈、破甲彈、碎甲彈、地雷、簡易爆炸裝置(IEDs)等反裝甲武器造成的爆炸導(dǎo)致受傷人員爆炸傷發(fā)生率高,尤其是創(chuàng)傷性顱腦損傷(TBI)發(fā)生率高居部位傷首位。據(jù)報(bào)道,美軍60%以上的爆炸傷出現(xiàn)TBI,其中大約80%為輕度TBI(mild-TBI)。由于輕度TBI傷員早期無特異腦損傷體征,出現(xiàn)以認(rèn)知、記憶障礙為主的精神障礙,常與創(chuàng)傷后應(yīng)激紊亂綜合癥(PTSD)混淆,早期救治時(shí)易被忽略。因此,為提高艙室爆炸傷的救治水平,有必要探討艙室爆炸的致傷機(jī)理,同時(shí)為防治艙室爆炸傷提供新的思路。 依照艙室爆炸的類型,艙室爆炸傷可分為艙內(nèi)爆炸和艙外接觸爆炸兩種類型。前者見于穿入艙室的彈頭爆炸或破甲彈金屬射流造成的傷害,后者見于裝甲防護(hù)能力強(qiáng)時(shí),反裝甲武器彈藥未能擊穿裝甲防護(hù)層,爆炸所造成的艙室內(nèi)人員損傷。以往認(rèn)為,艙外接觸爆炸主要造成艙內(nèi)乘員拋擲、碰撞,出現(xiàn)類似交通事故傷的低加速度、高位移的撞擊傷。為了減少艙外接觸爆炸傷的發(fā)生,目前裝甲車輛乘員大多由安全帶等固定裝置約束在座位上加以保護(hù)。但近來的研究發(fā)現(xiàn),艙外接觸爆炸造成的艙體高加速度(可達(dá)上萬g)可造成與艙體緊密接觸的人員肢體骨折、韌帶撕脫、斷裂、關(guān)節(jié)軟骨破碎等,同時(shí)艙體的快速變形產(chǎn)生的衍生空氣沖擊波也會(huì)引起臟器組織的損傷。但迄今尚不清楚艙室乘員顱腦是否存在損傷,以及這類損傷與記憶、認(rèn)知障礙的關(guān)系。 針對上述問題,本項(xiàng)研究在建立艙室外接觸爆炸傷實(shí)驗(yàn)?zāi)Ｐ偷幕A(chǔ)上,從以下兩部分探討艙室外接觸爆炸艙內(nèi)大鼠腦損傷特點(diǎn)和機(jī)理。 一、觀察艙室外接觸爆炸艙內(nèi)大鼠腦損傷特點(diǎn) 按正常成人與成年Spraque-Dawley(SD)雄性大鼠體積比,等比例縮小某型裝甲運(yùn)兵車,采用厚度為3.8mm的A級防彈鋼板作為材料,建造艙室。將大鼠固定在艙室內(nèi)座位上,取坐姿,引爆底板下方點(diǎn)爆源(400mg、800mg TNT當(dāng)量點(diǎn)爆源分別記為E1、E_2,對應(yīng)的致傷組分別為E1組、E_2組,正常對照組為N組),觀察傷后大鼠一般情況及腦損傷特點(diǎn),包括病理(鏡下組織細(xì)胞結(jié)構(gòu)、細(xì)胞凋亡、膠質(zhì)細(xì)胞反應(yīng)增生、腦含水量)、生化(腦損傷標(biāo)志物NSE、S-100B含量)以及神經(jīng)行為學(xué)(早期空間學(xué)習(xí)記憶)改變。 二、探討艙室外接觸爆炸艙內(nèi)大鼠腦損傷機(jī)理將艙內(nèi)座位懸空(與底板不接觸,阻斷加速度傳導(dǎo)),采用E_2作為點(diǎn)爆源,再按上述方法致傷(實(shí)驗(yàn)組為J組),觀察傷后大鼠腦損傷傷情變化,同時(shí)測量E1組、E_2組、J組座位加速度、大鼠頭顱加速度及大鼠頭顱位置空氣壓力,并分析其與大鼠腦損傷關(guān)系,以探討艙室外接觸爆炸艙內(nèi)大鼠腦損傷機(jī)理。 主要結(jié)果如下: 1.傷后大鼠均存活,麻醉清醒后反應(yīng)遲鈍。E_2組大鼠傷后立即出現(xiàn)短暫呼吸變緩、平均動(dòng)脈壓下降,其中4只出現(xiàn)短暫呼吸暫�，F(xiàn)象,持續(xù)時(shí)間(30-120)s。肉眼觀大鼠顱腦、脊髓及心、肺等內(nèi)臟器官無明顯挫傷、出血。光鏡下早期神經(jīng)元胞體縮小變形、胞核固縮,胞質(zhì)深染等急性壞死性改變,而后出現(xiàn)細(xì)胞核溶解,殘留細(xì)胞輪廓,見于脊髓前角運(yùn)動(dòng)神經(jīng)元、腦干核團(tuán)神經(jīng)元、大腦皮層、海馬的錐體細(xì)胞及小腦蒲肯野細(xì)胞,微血管周圍間質(zhì)疏松、淡染,其中傷后6h各組大鼠海馬CA1組織學(xué)損傷分級E_2組E1組N組,正常神經(jīng)元密度E_2組E1組N組(P0.01),傷后24h神經(jīng)細(xì)胞凋亡率E_2組E1組N組(P0.01),傷后168 h海馬齒狀回GFAP陽性細(xì)胞胞體肥大,突起增粗,細(xì)胞數(shù)E_2組E1組N組(P0.01)。電鏡下E_2組神經(jīng)元胞核水腫、內(nèi)質(zhì)網(wǎng)囊腔擴(kuò)張,核周隙擴(kuò)張,毛細(xì)血管內(nèi)皮及基膜破損、不完整,軸索水腫、脫髓鞘、髓鞘排列紊亂等。E1、E_2組傷后3h腦含水量增加,多于N組(P0.05,P0.01),6h后達(dá)到高峰,而后逐漸下降,168h后降至正常,6h、24h時(shí)相點(diǎn)E_2組腦含水量多于E1組(P0.01)。E1、E_2組傷后6h血漿NSE、S-100B濃度升高,大于N組(P0.05、P0.01),24h后達(dá)到峰值,E_2組大于E1組(P0.01),168h降至傷前水平。上述結(jié)果提示爆炸能量越大,艙內(nèi)大鼠腦損傷程度越重。 E_2組大鼠致傷后進(jìn)入定位航行訓(xùn)練期,在第1 d～4 d逃避潛伏期較N組延長(P0.05),晚1 d進(jìn)入平臺期,且在第6 d空間探索實(shí)驗(yàn)中,經(jīng)過平臺次數(shù)減少(P0.01),提示早期空間學(xué)習(xí)障礙。E_2組大鼠在定位航行訓(xùn)練期結(jié)束后致傷,在隨后空間探索實(shí)驗(yàn)中,跨越目標(biāo)象限時(shí)間與經(jīng)過平臺次數(shù)均明顯少于N組(P0.01),提示早期空間記憶障礙。 2.E1、E_2爆炸后艙室底板均無明顯變形,但座位加速度很高,作用時(shí)間很短,即“瞬間高加速度”。E1爆炸時(shí)座位加速度峰值、峰值上升時(shí)間及持續(xù)作用時(shí)間分別為(5745±1036)g、(1.41±0.28)ms、(6.87±0.58)ms,E_2爆炸時(shí)分別為(13109±1167)g、(0.81±0.14)ms、(11.08±1.43)ms。而E1爆炸時(shí)大鼠頭顱的加速度峰值、峰值上升時(shí)間及持續(xù)作用時(shí)間分別為(701±309)g、(0.78±0.18)ms、(1.00±0.14)ms,E_2爆炸時(shí)分別為(3383±935)g、(0.40±0.12)ms、(1.35±0.18)ms。以上結(jié)果提示座位加速度可傳至大鼠頭顱,并隨爆炸能量增加其加速度峰值增加、峰值上升時(shí)間縮短、持續(xù)作用時(shí)間延長。E1與E_2爆炸時(shí)艙內(nèi)大鼠頭顱位置最大壓力峰值、持續(xù)時(shí)間分別為(11.051±1.037)kpa、(25.0±1.4)ms與(19.250±2.179)kpa、(28.5±2.6)ms,結(jié)果證實(shí)衍生空氣沖擊波存在,且隨爆炸能量增加其壓力峰值增加、持續(xù)時(shí)間延長。將艙內(nèi)座位懸空后,E_2爆炸時(shí)座位加速度峰值、峰值上升時(shí)間及持續(xù)作用時(shí)間均很小,幾乎為零,即阻斷加速度對大鼠的作用,而衍生空氣沖擊波仍存在。此時(shí)J組艙內(nèi)大鼠在海馬CA1區(qū)神經(jīng)元損傷、腦含水量增多、血漿NSE、S-100B濃度升高、空間學(xué)習(xí)記憶障礙等方面較E_2組明顯減輕(P0.01),與N組無明顯差異(P0.05),提示主要致傷因素為座位加速度,衍生空氣沖擊波參與致傷,但作用很小。 結(jié)論: 1.艙室外接觸爆炸艙內(nèi)大鼠存在輕度彌漫性腦損傷,盡管大體形態(tài)改變不明顯,但鏡下病理、生化改變明顯,伴有短暫生命體征變化及早期空間學(xué)習(xí)記憶障礙,且損傷程度與爆炸能量呈正相關(guān)。 2.艙室外接觸爆炸艙內(nèi)大鼠腦損傷主要由座位高加速度所致。本實(shí)驗(yàn)中座位高加速度峰值很高(5745g～13109g),峰值上升時(shí)間很短(0.81ms～1.41ms),作用時(shí)間也很短(6.87ms～11.08ms)。爆炸能量越大,加速度峰值越高,峰值上升時(shí)間越短,作用時(shí)間越長,艙內(nèi)大鼠腦損傷程度越重。衍生空氣沖擊波參與致傷,但作用很小。 3.損傷機(jī)制考慮為爆炸后由于底板變形小,相當(dāng)一部分能量轉(zhuǎn)化底板、座位的加速度,經(jīng)大鼠與艙體接觸部位傳入體內(nèi)并向遠(yuǎn)處傳播,而由于軀干組織致密、變形較小,能量衰減少,以致更多能量通過軀干繼續(xù)傳遞,作用于遠(yuǎn)處組織(如脊髓、腦等)并引起損傷。 4.從本研究結(jié)果得到提示,艙室設(shè)計(jì)時(shí)既要防止乘員拋擲傷,也要注意由此可能帶來更嚴(yán)重的瞬間高加速度的致傷作用。
[Abstract]:In the war of Iraq , during the war in Afghanistan , the United States - based multinational force fighters mainly fought in combat cabins such as armored vehicles , and the explosive injury caused by anti - armoured weapons such as armored vehicles , bullet - breaking bombs , broken shells , mines and improvised explosive devices led to high incidence of explosive injury .


According to the type of explosion in the cabin , the explosion injury of the cabin can be divided into two types : an in - cabin explosion or an external contact explosion . The former is found in a warhead explosion or a bullet - breaking metal jet penetrating into the cabin , and the latter is found in the cabin in which the armor protection layer and the explosion are damaged . In the past , it is found that the high acceleration of the cabin body caused by the explosion of the cabin body can cause the injury of the organ tissue .


In view of the above problems , this study is based on the establishment of an experimental model of the explosion injury outside the cabin , and the characteristics and mechanism of the brain injury of the rat in vitro contact explosion cabin are discussed from the following two parts .


1 . Observation of the characteristics of brain injury in the explosion chamber exposed to the outside of the cabin


In normal adult and adult spraque - Dawley ( SD ) male rats , a class of armoured personnel carriers were reduced . A Class A bulletproof steel plate with a thickness of 3.8mm was used as the material to construct the cabin . The rats were fixed in the seats of the cabin , and the explosive sources ( 400 mg , 800mg TNT equivalent point explosion source were respectively designated as E1 and E _ 2 , and the corresponding wounding groups were E1 and E _ 2 respectively ) .


2 . To investigate the mechanism of brain injury in the rat brain injury induced by external contact explosion in the cabin , and use the E _ 2 as the point explosion source , and then the injury of the brain injury in the injured rats was observed by the method described above ( experimental group is J group ) .


The main results are as follows :


In group E _ 2 , the content of brain water was increased in group E _ 2 group ( P0.05 , P0.01 ) . The contents of NSE and S - 100B in the group E _ 2 were higher than those in group E _ 2 ( P0.05 , P0.01 ) . After 24h , the peak value was reached , the E _ 2 group was larger than that of the E1 group ( P0.01 ) , and the level of injury was decreased at 168 h . The above results suggested that the greater the explosive energy , the heavier the degree of brain injury in the rat .


In the experiment of space exploration , the time of crossing the target quadrant and the number of passing stages were significantly lower than that of the N group ( P0.01 ) , suggesting the early spatial memory impairment .


The peak of acceleration , peak rise time and duration of E _ 2 explosion were ( 5745 鹵 1 167 ) g , ( 0 . 81 鹵 0 . 14 ) ms and ( 1 . 35 鹵 0 . 18 ) ms , respectively .


Conclusion :


1 . There were mild diffuse brain injury in the explosion chamber outside the cabin , although the general morphological changes were not obvious , but the pathological and biochemical changes were obvious , with transient vital sign changes and early spatial learning and memory impairment , and the degree of injury was positively correlated with the explosion energy .


2 . The high acceleration peak of the seat was very high ( 5745g ~ 13109g ) and the peak rise time was very short ( 6.87 ms ~ 11.08 ms ) . The longer the peak rise time , the longer the peak rise time , the longer the action time , the heavier the degree of brain injury in the cabin .


3 . The damage mechanism takes into account the small deformation of the base plate after the explosion , the acceleration of the seat is transformed into the body through the contact part of the rat and the cabin body and propagates far away , and because the trunk tissue is compact , the deformation is small , the energy attenuation is reduced , so that more energy can continue to be transmitted through the trunk , and acts on the distant tissue ( such as the spinal cord , the brain and the like ) and causes damage .


4 . From the results of this study , it is suggested that when the cabin is designed , it is necessary to prevent the occupant from throwing the injury , but also to pay attention to the injury which may result in more severe transient high acceleration .

【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2011
【分類號】：R82

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