电击伤组织的超微结构观察

目的 观察电流传导路径上器官、组织的超微结构变化。 方法 对 SD大鼠进行实验性低电压电击。结果 触电部位皮肤的上皮细胞胞浆内基质凝固、膜系统断碎;骨骼肌肌小节出现异常收缩带;心肌的变化也较明显,可见局灶性溶解坏死并出现异常收缩带;电流传导路径上外周血管、神经的改变以血管明显,血管内皮细胞胞浆中出现空泡,中膜平滑肌可见溶解坏死,神经纤维仅见部分髓鞘松解。 结论 电击伤组织的超微结构变化可作为诊断电击死组织学变化的补充,为解决无明显皮肤电损伤的电击死案件提供形态学指标。同时也探讨了电击伤超微结构变化的形成机制。     

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。     

HCN4、Cx43在电击死者窦房结组织中的表达变化

目的研究电击死者心脏窦房结组织中超极化激活环核苷酸门控阳离子通道4(hyperpolarizationactivated cyclic nucleotide-gated cation channel 4,HCN4)及连接蛋白43(connexin43,Cx43)表达的变化。方法选择2010—2013年徐州医学院病理学教研室尸体解剖中有明确电流斑的电击死者34例作为电击死组,并设交通事故颅脑损伤死者20例作为对照组。应用免疫组织化学法检测HCN4和Cx43在心脏窦房结组织中的表达。结果 HCN4阳性细胞表达于窦房结细胞膜及细胞质中,Cx43阳性细胞表达于窦房结T细胞及心肌细胞的细胞膜及细胞质中。电击死组HCN4的表达高于对照组(P0.05),Cx43的表达低于对照组(P0.05)。结论电击死者窦房结组织中HCN4和Cx43表达的变化,说明电击死可能与心脏电生理的改变及冲动传导改变有关。     

生前电击与死后电击骨骼肌肌小节的长度变化

目的研究生前电击与死后电击的肌小节长度变化,为生前电击与死后电击的鉴别提供新的方法。方法12只兔随机分为对照I组、对照II组、电击死组和死后电击组。每组3只。对照I、II组与死后电击组兔分别从耳缘静脉注射空气30m l处死。对照I组处死后,于死后即刻取其后肢股四头肌;对照II组死后24h于相同部位取材;电击死组兔通220V交流电,通电致兔死后即刻取材;死后电击组于死后即刻通220V交流电4m in后,在相同部位取材。用透射电镜观察骨骼肌肌小节长度变化,对所得结果进行统计学分析。结果生前电击与死后电击骨骼肌肌小节均缩短,与对照组I相比,前者较后者缩短程度更甚(P=0.000);死后电击组与对照I组相比,仅轻微缩短(P=0.000),对照II组相比,缩短较为明显(P=0.000);对照II组较对照I组的肌小节显著伸长(P=0.000)。结论研究骨骼肌肌小节的长度变化有助于鉴别生前电击与死后电击。     

电击死大鼠皮肤超微结构及心肌HIF-2α、H-FABP的表达变化

目的 观察电击死大鼠皮肤超微结构,检测心肌细胞中缺氧诱导因子-2α(hypoxia-inducible factor-2α,HIF-2α)和心脏型脂肪酸结合蛋白(heart type-fatty acid-binding protein,H-FABP)的表达变化,为电击死的法医学鉴定提供依据.方法 建立大鼠电击模型,将...     

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。     

意外电击死21例法医病理学分析

皮肤电流损伤是诊断电击死的主要依据。经对21例意外电击死案例进行系统法医病理学检查后发现：肉眼具典型电流斑者仅6例（29％），光镜下形态改变与其他学者描述基本一致。非典型电流斑形态多样化，以单纯性表皮剥脱多见。体内器官病理学变化缺乏特异性。     

电击死心肌组织中纤维连接蛋白的实验观察

目的 研究电击死大鼠心肌组织中纤维连接蛋白的表达,为电击死和电损伤的鉴定提供一定依据。方法 取大鼠12只,实验组与对照组各6只。应用SABC法对实验组与对照组进行免疫组化研究。同时应用常规染色作比较。结果 电击死心肌内出现纤维连接蛋白的阳性,与对照组差别有意义(P<0.01)。结论 心肌组织中纤维连接蛋白的强阳性表达对电击死的法医学鉴定有一定参考价值。     

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。     

电击死兔骨骼肌及心肌HSP70 mRNA和c-fos mRNA表达

目的 研究电击死兔骨骼肌与心肌HSP70 mRNA和c-fos mRNA-表达变化。探究生前电击与死后电击的鉴别方法。方法 15只新西兰兔,随机分电击死组、死后电击组和对照组,每组5只,用荧光RT-PCR技术检测骨骼肌与心肌热休克蛋白70（HSP70） mRNA与c-fos mRNA表达水平,对所得结果进行统计学分析。结果 生前电击兔骨骼肌及心肌HSP70 mRNA与c-fos mRNA表达高于死后即刻电击者（P〈0．05）。结论 检测骨骼肌及心肌HSP70 mRNA与c-fos mRNA表达变化有助于于生前电击与死后电击的鉴别。     

青壮年猝死综合征心肌心钠素免疫组化研究

研究青壮年猝死综合征病理形态学诊断依据。应用免疫组化LSAB,观察10例SMDS及10例非心性死亡对照组死者ANP变化情况。结果发现,SMDS中7例ANP呈阴性,3例呈弱阳性;10例非心性死亡ANP呈强阳性。研究表明,SMDS死者心房内ANP数量减少是导致死亡的重要因素,可通过ANP免疫组化观察找到SMDS死亡的形态学依据。     

Homicidal electrocution disguised as an accidental death

Deaths due to electrocution are mostly accidental. Homicide by electrocution is rarely reported in the literature. However, the location and pattern of the electrocution wound can raise concern for a possible homicidal manner of death. We are reporting an unusual case wherein the dead body of a middle-aged man was found lying in a suspicious condition on the roadside of desolated area. There were circumferential, grooved electrocution lesions over the left and right second toes with oval electrocution lesions on the medial aspects of both the left and right third toes. There were split lacerations over the right high parietal region, right pinna, and forehead. There was avulsion of the nail of the left thumb. Pressure abrasion was consistent with a ligature mark on the lower part of the left leg. The locations and pattern of these injuries raised the possibility of torture infliction. Death was attributed to electrocution, which was confirmed by histopathology. Autopsy findings and possible inferences were furnished to the police. This case highlights the careful observation of different characterizations and locations of the wounds and deducing inferences about the possible manner of death. This information can be useful to investigating agencies.     

Connexin 43, angiotensin II, endothelin 1, and type III collagen alterations in heart of rats having undergone fatal electrocution

Death due to accidental electrocution occurs frequently. The aim of this study was to investigate alterations in cardiac connexin 43 (Cx43), angiotensin II (Ang II), endothelin 1 (ET-1), and type III collagen associated with fatal electrocution.Twenty-four Sprague-Dawley rats were divided into control, fatal electrocution (220 V, 50 Hz, 60 seconds), and electrical injury (220 V, 50 Hz, 60 seconds) groups. Animals were deeply anesthetized with sodium pentobarbital before each treatment, with the anode connected to the left foreleg and the cathode to the right hindleg, followed by cervical dislocation. Control animals received cervical dislocation alone. Immunohistochemical analysis was performed to evaluate the cardiac protein expression of Cx43, Ang II, ET-1, and type III collagen. Sections were analyzed by digital image analysis.The expression of Cx43 was significantly reduced after fatal electrocution, with the integrated optical density also lower when compared with control (P < 0.05). Expression of both Ang II and ET-1 was significantly increased after fatal electrocution, supported by integrated optical density when compared with control (P < 0.05). But no significant difference was found in type III collagen expression between the fatal electrocution group and the control group.In summary, cardiac protein expression of Cx43, Ang II, and ET-1 was found to be significantly altered with fatal electrocution, suggesting that these 3 proteins may be important underlying mechanisms of death during fatal electrocution. The current findings indicate that such alterations would be reflected in abnormal cardiac function and a possible cause of sudden death.     

Study on electrocution death by low-voltage

Seven cases of electrocution death by low voltage (<80 V) were studied. Autopsy was carried out and the death scene was investigated. The conditions for low-voltage electrocution death, the state of the victim at the time of electrocution, postmortem examination and the nature of the electricity is discussed. It was pointed out that low-voltage electrocution was related to the nature of electricity, individual characteristics and environment conditions.     

Experimental evaluation of rigor mortis. VII. Effect of ante- and post-mortem electrocution on the evolution of rigor mortis

The influence of electrocution on the evolution of rigor mortis was studied on rats. Our experiments showed that: (1) Electrocution hastens the onset of rigor mortis. After an electrocution of 90 s, a complete rigor develops already 1 h post-mortem (p.m.) compared to 5 h p.m. for the controls. (2) Electrocution hastens the passing of rigor mortis. After an electrocution of 90 s, the first significant decrease occurs at 3 h p.m. (8 h p.m. in the controls). (3) These modifications in rigor mortis evolution are less pronounced in the limbs not directly touched by the electric current. (4) In case of post-mortem electrocution, the changes are slightly less pronounced, the resistance is higher and the absorbed energy is lower as compared with the ante-mortem electrocution cases. The results are completed by two practical observations on human electrocution cases.     

An unusual case of high-voltage electrocution of a truck driver due to inadvertent contact of the truck with an overhead wire

Electrocution deaths are mostly accidental. However, reconstruction of events in unusual electrocution death is challenging. This article reports an accidental death due to electrocution in a highly unusual circumstance, in which a truck driver reversing his vehicle was electrocuted when his truck inadvertently touched an overhead high-voltage wire. The electric injury marks were present over the sole of the right foot. The scene investigation revealed that the high-voltage wire was loose and was below the level of the prescribed height. The truck was passing over an elevated area made up of dirt and stone. The interior of the cabin of the truck revealed a few non-insulated metallic areas over the floor of the truck, between the accelerator and the brake, which were attributed as the sources of entry of electricity into the body. The electric injury marks were different than those usually seen in high-voltage electrocution as there was an intermediate object (truck) involved, and the contact period between the truck and the electric wire was minimal. This fatality was attributed to the non-proper insulation of the interior of the truck, the negligent driving of the truck driver over the elevated surface, and the loose high-voltage wire without proper maintenance.     

Endothelial cell membrane perforation of aorta and pulmonary artery in the electrocution victims

Some electrocution deaths occur without detectable current marks on the skin, making forensic examination to determine the true cause of death more difficult. Because arterial thrombosis was a frequent finding in victims of electrocution, we investigated injury to the endothelium of the aorta and pulmonary artery with a scanning electron microscope in five cases of death known to be caused by electrocution. We found large pores on the surface of endothelial cells of the aorta and pulmonary artery in those who died of electrocution, but no endothelial membrane perforation was found in those who died of cardiac diseases. These findings were present within 12h after death. Therefore, scanning electron microscopic evidence of endothelial perforation in the aorta and pulmonary artery could be a useful marker to identify electrocution for those victims without detectable current marks on the skin.