Huang Quan-Yong, Chen Yu-Chuan, Liu Shui-Ping
Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Am J Forensic Med Pathol. 2012 Sep;33(3):215-21. doi: 10.1097/PAF.0b013e31823f04eb.
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.
意外触电致死的情况屡见不鲜。本研究旨在探讨与致命触电相关的心脏连接蛋白43(Cx43)、血管紧张素II(Ang II)、内皮素1(ET-1)和III型胶原蛋白的变化。将24只Sprague-Dawley大鼠分为对照组、致命触电组(220 V,50 Hz,60秒)和电损伤组(220 V,50 Hz,60秒)。每次处理前用戊巴比妥钠将动物深度麻醉,阳极连接左前肢,阴极连接右后肢,然后进行颈椎脱臼。对照组动物仅接受颈椎脱臼。采用免疫组织化学分析评估Cx43、Ang II、ET-1和III型胶原蛋白的心脏蛋白表达。切片通过数字图像分析进行分析。致命触电后Cx43的表达显著降低,与对照组相比,积分光密度也较低(P < 0.05)。致命触电后Ang II和ET-1的表达均显著增加,与对照组相比,积分光密度支持这一结果(P < 0.05)。但致命触电组与对照组III型胶原蛋白表达无显著差异。综上所述,发现致命触电后Cx43、Ang II和ET-1的心脏蛋白表达显著改变,表明这三种蛋白可能是致命触电死亡的重要潜在机制。目前的研究结果表明,这种改变会反映在心脏功能异常上,可能是猝死的原因。