电击后心脏损伤的实验研究

将电击器电路连接家兔左前肢和右后肢，用200v5mA交流电定时电击，制造电击死和电击伤时心脏损伤的动物模型。结果显示：电击死前ECG出现室颤波，光镜下心肌纤维广泛断裂，间质出血，小血管周围水肿．心肌灶性坏死，心房心肌坏死累及心内膜时有微小附壁血栓形成；房室结细胞核空泡变，胞浆深嗜伊红性；电镜下心肌纤维闰盘撕裂；心肌Ⅰ带消失，肌节缩短，超收缩带（Hypercontractionbands）形成，或Ⅰ带扩大，肌节拉长，Z线移位；肌原纤维溶解等。电击伤动物出现心肌散在性坏死灶内炎性浸润，灶性心内膜炎，小冠状动脉狭窄或闭塞。传导系统炎性浸润。本实验对电击死的法医学鉴定和非致死性电击伤心脏并发症的诊断提供病理学基础。     

水、油污中无电流斑电击死大鼠皮肤和心肌的病变

目的探讨水中、油污中无电流斑电击死法医学鉴定的病理形态学依据。方法 SD大鼠28只,分为水中、油污中无电流斑电击死各1组,典型电流斑组、正常对照组、死后电击组、死后水中、油污中电击各1组共7组。采用肉眼、光镜及投射电镜观察水中、油污中无电流斑电击死大鼠皮肤和心肌组织病理学改变,并与其它各组进行比较。结果采用肉眼观察,生前水中、油污中无电流斑电击死大鼠皮肤未见明显电流斑。普通光镜观察,可见电击中心部位表皮变性坏死、脱落,表皮细胞变薄、致密,表皮细胞或/和毛囊、汗腺、皮脂腺发生极性化改变。电镜观察,透明层和角质层分离脱落,基底细胞肿胀、细胞器减少、核固缩,汗腺导管上皮肿胀,棘细胞中粗面内质网扩张融合成泡状,线粒体肿胀空泡化;但光镜与电镜的变化与生前电击死比较不明显、典型。而死后电击组皮肤则无明显病理学改变。实验各组大鼠心肌的改变与皮肤改变类同。结论采用光镜和投透射电镜观察在潮湿环境中电击死的组织病理学改变,可为无电流斑电击死提供依据。     

电击死亡心肌收缩带的研究(附10例)

<正> 目前在电击死法医学鉴定中,主要是依据皮肤的电流斑,但在实际案例中常遇到皮肤无电流斑或电流斑不显著,给鉴定带来困难。因此必须研究电击对其他脏器损伤的证据。本文对电击死亡心肌收缩带在法医学鉴定中的意义进行了研究。     

电击死大鼠心脏超微结构及HSP70、HIF-1α表达变化

目的观察电击死大鼠心脏超微结构及热休克蛋白70(heat shock protein 70,HSP70)、低氧诱导因子-1α(hypoxia inducible factor-1α,HIF-1α)的表达变化,探讨其是否能作为电击死法医学鉴定的依据。方法将72只SD大鼠随机分为电击死组、死后电击组和对照组。通过透射电镜观察电击死大鼠心肌超微结构的改变,并采用免疫组织化学技术观测心肌HSP70和HIF-1α的表达变化。结果电击大鼠心肌细胞肌原纤维断裂,线粒体嵴和膜溶解消失,Z线、M线排列紊乱。HSP70和HIF-1α在电击死组呈强阳性表达,与死后电击组、对照组比较差异有统计学意义(P0.05)。结论 HSP70和HIF-1α在电击死组表达明显上调,有望作为电击死的诊断参考指标。     

大鼠电击死心脑肺及皮肤超微结构的改变

目的 观察电击致死大鼠的心、脑、肺、皮肤超微结构形态学改变，寻找电击死的法医学鉴定依据。方法 大鼠12只，其中电击致死6只，另6只对照；取心、脑、肺、皮肤，用戊二醛固定、锇酸染色后透射电镜观察。结果 所取组织细胞均见明显细胞凋亡样改变，其中红细胞肿胀变形，充填整个毛细血管管腔。结论 心、脑、肺、皮肤组织细胞与血管内皮细胞的超微结构形态改变对鉴定电流死有参考价值。     

23例电击死尸检取材和法医鉴定方法研究

目的在前期动物实验基础上,结合电击死人体尸检病理组织学观察,确定电击死鉴定最佳的组织取材部位。方法选取23例明确"手-足路径"电击死者,明确死于交通事故颅脑损伤和冠心病猝死者各10例为对照组。所有案例提取双腕上前内侧、双踝上后部等部位软组织,观察并分析其骨骼肌(Sk MCs)和动脉血管平滑肌细胞(ASMCs)的核轴比变化。结果 23例电击死案例,年龄19~59岁,男性19例、女性4例;高压电击死3例,日用低压电击死20例;7例出现典型电流斑(31.18%);5例出现胸膜电击纹(22.7%)。电击死组的前腕、内踝的Sk MCs和ASMCs细胞核拉长、扭曲,呈波浪样、栅栏状排列,其核轴比与对照组相同部位比较,有显著性差异(P<0.001),而且ROC曲线分析,Sk MCs和ASMCs的核轴比的诊断临界值为分别4.84、3.81。结论在"手-足路径"电击死的最佳取材部位应为机体电流路径中最狭窄位置,即腕、踝部位,该部位Sk MCs和ASMCs细胞核的极向性拉长、靠近呈串珠状或直线状排列,为最具特征性和诊断价值的电损伤形态学变化。     

电击伤最佳病理取材部位的初步研究

目的探讨日常低电压电击后机体电流通路上极向化等病变规律和最佳病理取材部位。方法SD大鼠随机分为电击组和对照组,建立左前爪-右后爪路径220V电击大鼠模型,取电极接触处皮肤、四肢血管、神经和周边组织及腹腔大血管,常规HE染色病理组织学图像分析。结果电极接触处皮肤基底细胞(skinbasalcell,SBC)核明显极向化改变,长/短径比值与对照组比较差异高度显著,P<0.001;电流通路上腕和踝部血管及腹主动脉内皮、平滑肌细胞核的极向化与对照组比较,差异显著,P<0.05,其中腕和踝部病理改变最明显;周围骨骼肌细胞核的长/短径比值无明显规律性。结论在电击死中最常见的“手-足通路”,腕、踝部血管可能为病理取材的最佳部位。同时,由于腕和踝部距离手脚掌较远,直接接触热源和化学试剂等其他可能引起“极向化”改变的因素机会少,因此,腕和踝部血管及其周边组织的极向化改变更具有电损伤的特异性。     

电击死大鼠心肌细胞磷脂变化的研究

目的探讨无电流斑与有电流斑电击死心肌组织磷脂分布。方法 15只SD大鼠,无电流斑和有电流斑各6只,对照组3只。实验组通过自制电击装置通电致死,对照组采用脱颈处死。实验组和对照组大鼠死后0h、12h、24h三个时间段取心肌组织固定和冷冻,对其分别进行制片HE染色和磷脂染色。结果电击死均可见心肌纤维断裂、波浪状改变,血管内皮细胞极性化改变,部分心肌间质少量出血。磷脂染色:电击死0h、12h心肌细胞膜磷脂缺失,随时间延长,磷脂缺失程度加重。对照组仅可偶见单个磷脂位于细胞间质或少量心肌细胞膜磷脂缺损。死后24h,电击组、对照组均可见大面积心肌细胞膜磷脂缺失。结论心肌细胞膜磷脂染色可有助于电击死诊断,但死亡时间达到24h左右则诊断价值不大。     

胸腔“浆膜电击纹＂4例分析

近年来随着电力事业的迅猛发展和各种电器的广泛应用,电击伤亡事件呈明显上升趋势。对于缺乏电流斑和皮肤电击纹等电击伤特征性变化的死者,目前,法医鉴定时主要靠综合现场案情调查和系统尸检结果,作出排除性结论[1-2]。笔者在工作中发现4例电击死者胸腔壁层浆膜下,出现较特异的     

血管电损伤的实验研究

观察电击后血管病理改变的规律及特点 ,探讨其损伤的发病机制和诊断电击伤 (死 )的价值。采用Wistar大鼠复制血管电击伤模型 ,通过HE、GS、Weigert弹力纤维染色和α actin免疫组化染色 ,观察电击后不同节段血管的病理变化。结果表明 :(1)电击后血管的损伤范围和程度均较其周围大 ;(2 )电击部位的血管常发生全层凝固性坏死 ,血管周围骨骼肌、脂肪细胞广泛坏死 ,大腔隙形成 ;距电击部位越远损伤越轻 ,血管损伤局限于管壁中内层 ,而血管周围组织相对完好 ;(3)光镜下 ,血管内皮细胞不同程度坏死、脱落 ;平滑肌肌浆凝聚 ,呈嗜碱性 (异染 ) ,胞核深染 ,扭曲伸长呈栅栏状排列 ,细胞内外大量汽化空泡形成 ,肌层中弹力纤维减少 ,网状纤维相互融合增粗、断裂 ,呈串珠状改变。TEM下见血管内皮细胞、平滑肌细胞内线粒体、内质网不同程度肿胀与扩张 ,甚至空泡化改变 ,平滑肌肌丝溶解 ,形成低电子密度区 ;汽化空泡边界清楚 ,无膜性结构 ,内无细胞器 ;SEM下见血管壁及腔面粗糙大小不等的腔隙形成 ;(4 ) 2 2 0V组血管的病理改变与 10 0 0V组相同 ,只是损伤程度较前者轻。电击后血管的病理改变是电热效应与电场作用的共同结果 ,血管的病理改变可以作为一种确证电击死的重要依据     

海洛因成瘾大鼠心电图及心肌超微结构改变的研究

目的探讨海洛因成瘾大鼠心电图及心肌超微结构的改变,为海洛因对心脏的损害机制提供研究基础。方法建立大鼠海洛因成瘾模型,观察心电图、HE染色及心肌超微结构改变。结果大鼠海洛因成瘾组心电图改变明显,主要表现在心率减慢、P波及T波压低、时间延长,S-T段压低、时间延长,QT间期延长,上述差异有统计学意义(P<0.05),提示心肌损伤、心肌缺血及心室功能下降。电镜改变主要表现在核浓缩,核变小,核膜皱缩,染色质凝集成块,线粒体嵴排列紊乱、消失及空泡变等,提示海洛因可造成心肌细胞超微结构的病理改变。结论海洛因对心肌可造成损害,并且心肌超微结构改变提示心肌凋亡可能是海洛因造成心肌损伤的机制之一。     

Study on the changes of electrocardiogram and ultrastructural in heroin dependence in rats

OBJECTIVE: To study the changes of electrocardiograms (ECG) and myocardial ultrastructure in heroin dependence in rats, in order to reveal the mechanisms of the myocardial injury by heroin. METHODS: Establish heroin addict model in SD mice, investigate the changes in electrocardiograms, HE staining and myocardial ultrastructure. RESULTS: The electrocardiograms of the addict group had prominently changes, main expressions: heart rate decreased, P wave and T wave amplitude reduced and duration increased, S-T reduced and duration increased, QT interval prolongation, these changes indicated that myocardium had been injured, myocardial ischemia, ventricle function declined. These difference was significant (P<0.05) between before inject heroin and after inject heroin. Transformations in the ultrastructure: nuclear concentrate, reduce, nuclear membrane shrink, chromatin agglutinate, mitochondria cristal had disorder formation, disappeared or hollowed, these indicated that heroin could cause pathological changes in myocardial ultrastructure. CONCLUSION: Above-mentioned changes indicated that heroin can injure myocardium, and the changes of myocardial ultrastructure suggested that myocardial apoptosis may be one of the mechanisms of the myocardial injury by heroin.     

海洛因戒断大鼠位置偏爱及海马神经元膜电性质的变化

目的 研究海洛因戒断期大鼠的位置偏爱性和海马CA1区神经元电生理特性,并探讨行为变化与神经元膜电性质变化之间的关系。方法 制作海洛因慢性给药戒断大鼠模型,对大鼠Y型迷宫位置偏爱行为及其海马CA1区神经元膜电特性,以及电镜下海马皮质突触结构的变化进行观察,并与对照组比较。结果 海洛因慢性给药戒断期,大鼠Y型迷宫位置偏爱显著增强(P<0.01),其海马CA1区神经元静息膜电性质,与对照组相比无显著差异(P>0.05),但动作电位(AP)半幅时程和10％-90％衰减时间缩短(P<0.01);兴奋性突触后电位(EPSP)幅值和曲线下面积增大(P<0.01)。电镜下见戒断组动物海马皮质神经突触间隙较对照组变窄,前膜和后膜内电子致密物聚集,密度增高。结论 海洛因慢性给药戒断模型,可引起大鼠明显的位置偏爱,且在不改变静息膜电特性的前提下,海马CA1区神经元AP和EPSP特性及突触结构产生了相应的改变。     

Ultrastructural changes in dermal pig skin after exposure to heat and electric energy and acid and basic solutions

In order to describe the ultrastructure of the histopathological changes in dermis after exposure to electrical energy, heat energy and acid and basic solutions the skin of fully anaesthetized Danish Landrace pigs were exposed to direct current, heat (80 degrees C and 450 degrees C) and acid and basic solutions. Biopsies were obtained immediately after the exposure from all types of injury. Biopsies from the cathode areas biopsies were also taken on day 1 and day 2.5 in order to describe the initial calcium deposits. Homogeneous collagen fibres without any birefringence from heat exposed areas were ultrastructurally composed of filamentous materials. Collagen fibres with fine densely spaced cross-striation from cathode areas and areas exposed to basic solutions were shown ultrastructurally to consist of parallelly arranged collagen fibrils with regular waves. It is concluded that the cross-striation of the collagen fibres observed in polarized light are due to a periodic change in the orientation of the fibres seen as waves of the fibres. The ultrastructure of dermal cells were similar to that of epidermal cells following the different types of influence. Characteristically the nuclei were condensed following heat and more electron-lucent following direct current (d.c.) and acid and basic solutions. In cathode areas and areas influenced by basic solutions the electron-lucent nuclei contained fine fibrils. The ultrastructural study supports the suggestion from light microscopic studies that the morphology of anode and cathode lesions shows resemblance to acid induced and basic induced lesions, respectively. Apatite crystals were observed on day 2.5 at the periphery of the collagen fibrils and in the matrix of elastic fibres.     

Postmortem changes in electrical resistance of the gastric wall during the early postmortem period in rats.

A simple and reliable technique was employed for measurement of (dc) electrical resistance of the gastric wall of rats. Tissue resistance decreased linearly (r = -0.87; P less than 0.001) from 66.1 +/- 12.1 kOhm/cm2 immediately following death to 23.3 +/- 3.5 kOhm/cm2 at a postmortem interval of 24 h. These changes are believed to reflect progressive postmortem changes in the physical dimensions of the intercellular space and/or changes in electrical conductivity of the intercellular/extracellular fluids.     

Electrical and thermal injuries in pig skin — Evaluated and compared by light microscopy

The morphology of pig skin after electrical (el) and thermal exposure was studied in order to find methods applicable for disclosing electrical torture.Biopsies from pig skin exposed 24 hours earlier to either heat or electrical current under general anesthesia were studied by light microscopy. The amount of energy used of either type ranged from about 6 to about 100 joule deposited on two circular areas of the skin measuring 12 mm in diameter.In sections stained with hematoxylin and eosin alterations were found in heat-influenced specimens following the administration of moderate and large doses of energy. Changes were observed in el-influenced specimens also after the administration of low amounts of energy, which did not lead to macroscopical changes in the skin. The two types of energy induced different patterns of alterations inside the epidermis. The most characteristic change following heat exposure was the presence of a granular or fibrillar eosinophilic cytoplasm and subepidermal clefts, while el-expoure often produced white homogeneous cytoplasm and shadowy nuclei (“white necrosis”) in the attached epidermis. The individual changes could be produced by both types of injury, but to a highly different degree. However, the alteration classified as “vesicular nuclei” was only observed in el-damaged skin. The dermis from the more severely injured skin of both groups showed a homogeneous appearance (“necrosis”). While the changes of epidermis and dermis in response to heat were diffusely distributed, the changes created by electrical injury were often present in segments. By electrical damage homogeneous areas with loss of stainability and shadowy nuclei were occasionally observed in sweat glands, hair sheaths and in vessel walls, structures which are suggested to serve as conductors for the electrical current. “Vesicular nuclei” were observed in similar structures.Some of the findings may be associated with differences in intensity of energy during exposure to heat and electricity. Furthermore, the existence of different biological patterns following the two types of exposure should be considered. The studies are being continued to elucidate these basic questions, and to study further the medical diagnostic potential of examining skin biopsies from tortured individuals.     

大鼠死后皮肤傅里叶变换红外光谱变化与死亡时间的关系

目的运用傅里叶变换红外(Fourier transform infrared,FTIR)光谱技术分析大鼠死后15d内背部皮肤的光谱变化,以此推断死亡时间。方法大鼠麻醉后颈椎脱臼处死,置于温度为25℃、湿度为50%的环境中,分别于不同时间点提取其背部皮肤,收集红外光谱数据,并利用机器学习技术对数据进行分析。结果大鼠死后背部皮肤组织光谱吸收峰的峰位未发生明显改变,其强度随死亡时间延长而发生变化;偏最小二乘(partial least squares,PLS)回归构建的死亡时间推断模型决定系数(R2)为0.92,预测均方根误差为1.30 d。根据模型中的变量投影重要性(variable importance for projection,VIP)指标确定推断死亡时间的贡献波段为1760~1700cm-1、1660~1640cm-1、1580~1540cm-1和1460~1420cm-1。结论应用FTIR技术检测大鼠死后皮肤组织的光谱学改变,为死亡时间推断提供了一种新的思路。     

家兔低压电击伤后血清LDH和HBDH活性变化

目的研究家兔非热低压电击伤后不同时间乳酸脱氢酶（lactate dehydrogenase,LDH）和羟丁酸脱氢酶（hydroxybutyrate dehydrogenase,HBDH）活性的变化．为I临床和法医学非热电击伤提供诊断依据。方法健康新西兰大白兔40只,随机分为对照组和电击伤后7个时间点的实验组,每组5只。实验组使用本室已建立的非热低压电击伤方法处理,电击后各实验组动物按照预定时间点麻醉后抽取5mL心室血．测定血清LDH,HBDH酶活性。结果在非热低压电击伤后家兔目标血清酶活性发生了动态变化,有一定规律性,其中LDH活性在电击伤后4、12h和1、2、3d明显升高（4、12h和1d P〈0．01;2和3d P〈0．05）;HBDH活性在电击伤后2和3d明显升高（P〈0．05）;电击组HBD肌DH比值在2、4和12h与对照组比较显著降低（P〈0．01）。结论动态监测LDH、HBDH活性,可为非热电击损伤的诊断,损伤时间推断提供理论依据。     

Skin changes following defibrillation. The effect of high voltage direct current

Previously, electrical injuries have been suggested caused only by the concomitant heat developed during the passage of an electrical current. Recent experimental studies on fully anesthetized pigs and the study of one human case have, however, shown typical electrical alterations. The purpose of the present study was further to evaluate the histology of electrically induced changes in the skin in humans. In addition, supplementary in vivo methods for evaluation of skin changes as high-frequency ultrasound and Raman spectroscopy were used. The skin of 11 patients treated with a defibrillation of the heart was examined for macroscopic changes, the skin of eight of them also for histologic changes and for changes observable via supplementary methods. Immediately and 7 days after the defibrillation, fractions of a narrow red ring were observed along the periphery of the tin-foil electrode. Epidermis showed signs previously observed following electrical influence: segmental alterations often related to the openings of sweat ducts, darkstaining or "empty" nuclei and homogeneous cytoplasm, eosinophilic or pale. Dermis did not show the specific sign of electrical influence: deposits of calcium salts on dermal fibres, neither via histologic examination nor via high-frequency ultrasonography and Raman spectroscopy. Fractions of a narrow red ring along the periphery of the electrode showing histological signs of electric influence in epidermis thus appear to be characteristic of high voltage electrical injury.