Skip Navigation LinksHome > September 2012 - Volume 33 - Issue 3 > Connexin 43, Angiotensin II, Endothelin 1, and Type III Coll...
American Journal of Forensic Medicine & Pathology:
doi: 10.1097/PAF.0b013e31823f04eb
Original Articles

Connexin 43, Angiotensin II, Endothelin 1, and Type III Collagen Alterations in Heart of Rats Having Undergone Fatal Electrocution

Huang, Quan-Yong MD*†; Chen, Yu-Chuan MD*; Liu, Shui-Ping MD*

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Abstract: 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.

© 2012 Lippincott Williams & Wilkins, Inc.


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