| Objective: Electrical injury (or death from electricity) is one of the familiar cases in legal medical practice; the current marks and metallization of skin is the most important diagnostic gist. However, the typical change of skin is so unusual in cases that its application in legal medicine is limited treatly. The heart, with high frequency of electro-physilologic activity, is sensitive to current. Electric shock, especially lethal electric shock, that always induce a serious of pahtophysiologic changes to happen in it. For the value of these pathophysiologic changes, there is different view on it in legal medicine. In order to understand its value in legal medicine, we studied it from pathologic changes and gene expression. Methods:1. The model of injured heart caused by electric force was replicated on Wister rats by 50Hz, 220V (150-200mA) current for 20second. 2. Excuted all rats by decapitation and took out the heart tissue from it at different time (30min, 1hour, 2hour, 3hour, 6hour, 12hour, 1day, 2day, 3day, 6day and 12day), then stored respectively the heart into 10%formalin and 4%glutaraldehyde for regular slice and ultra-slice, the slices were stained by HE, Masson, HBFP, FN and TUNEl for lighting microscope observation, and the ultra-slices were used to transsion electron microscope observation. 3. Detected the gene expression pattern of heart at 3 hour after it was injured by current by BioStar-40 oligonucleotide microarray. 4. Investigated the role of expression of PEG-3, α-fibrinogen, APPILS and Hyal2 at different time (1hour, 2hour, 3hour, 6hour, 8hour, 12hour, 1day, 2day, 3day, 6day, 12day). Results:The pathological changes observed by LM as follows: From 30 minture to 6 hour, poly-loci of myocardial cells denaturalization, necrosis and fragmentation, partial cells showed "wave-like" array and contraction bands necrosis; cytoplasm exhibiting homogenous and eosinophilic change, blurred cross striation; nuclear dakstaining, distorting, strenching and vacuolization; the myocardial interval broaden, edema and scattered bleeding; arteriole enlarging, nuclear of endothenial cells darkstaining, swelling, eosinophilic change of soomth cells, and hemaglutination; HBFP also showed multi- loci of ischemic myocardial cells. From 12hour to 3day, the scope of necrotic myocardial cells increasing, edema of the myocardial cells becoming more obvious, the little bands of fascle interval increasing and the transect of myocardium exhibited "sieve-like" change; partial myocardial cells dissolution and nuclear disappearance; vessel enlarging, nuclear of endothenial cells denaturalization, swelling and falling off, large number of red cells adhering on the wall of vessel, some neutrophil polymorphs aggulation and little of them leaked from vessel, transparent thrombus formation; a little loci of fibroblast and epimysium cells increasing. From 6 to 12 day,the scope of necrosis was lager than previous observied, partial fibroblast and epimysium cells increasing, large number of fiber increased in the myocardial interval of cells (Masson dyeing), and poli-loci of fiber insteaded necrotic myocardium. Notable, there wasn't obvious inflammatory response in all the pathological process, differented from the results observed by other studies. The cytoplasm of damaged myocardial cell was FN Positive, and undamaged cells were negative. At 30 min, the FN positive loci appeared in the central myocardium, and negative in outer and inner layer of myocardium. From 1hour to 2day, more and more FN positive cells appeared in all layers of myocardium, including outer and inner layer of myocardium. From 3 to 12 day, the FN positive cells decreased. The nuclear of damaged cell was TUNEL dyeing positive, and negative in undamaged cells. From 30 min to 2day, the positive cells increased, and from 3day to 12 day, the positive cells decreased. The ultrastructural changes by TEM the pathological change of mitrochondria was mainly at 30min after the heart injured by current, a mass of crests fragmentation and dissolution, mitochond...
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