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      실험적으로 일이킨 백서에서의 바이러스성 심근염에 대한 연구 = Experimentally Induced Viral Myocarditis in Mouse

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      https://www.riss.kr/link?id=A3306738

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      Background: The authors injected EMC virus (Encephalomyocarditis virus) to induce viral myocarditis in ICR mice in order to study the survival rate and serial histopathologic change of viral myocarditis according to duration. Methods: Seventy adult ma...

      Background: The authors injected EMC virus (Encephalomyocarditis virus) to induce viral myocarditis in ICR mice in order to study the survival rate and serial histopathologic change of viral myocarditis according to duration. Methods: Seventy adult male ICR mice of 8 to 10 weeks were used for experiment. Among 70 mice, 40 mice (Group I) were used to observe survival and 30 mice (Group II) were used to see serial histopathologic change (Each 5 mice were killed before and 5, 10, 20 days after virus injection). The hearts of animals were fixed in 10% buffered formalin and routinely processed. Hematoxylin & Eosin stain and Masson trichrome stain were done to observe inflammation and fibrosis. Results: 1) In Group I, 1 mouse died at each 2, 4, 5, 6 day after virus injection, and 4 mice died at 7 day and 2 mice died at 10 and 11 day. Total 10 animals among 40 died (mortality: 25%), and showed peak death period at 4-7 days, 2) In Group II, at 5th, 10th, 20th day after virus injection, average inflammatory grade in the myocardium were 1.8, 3.4, 2.0, respectively. 3) Histologic findings revealed monouclear cells infiltration, myofiber necrosis & degeneration. These changes occur multifocally rather than diffusely. Inflammation was most severe at 10 days. 4) Fibrosis was increased at 20 days after virus injection compared to early phase of myocarditis. Distribution of fibrosis is relatively parallel with the area of inflammation, but not with the degree of inflammation. 5) In some cases, dilation of both atriums and ventricles and thrombosis accompaning severe pulmonary congestion and edema were observed, indicating possible transition to dilated cardiomyopathy. Conclusions: It is considered that this experimental animal model may be useful not only to study the pathogenetic mechanisms of viral myocarditis but also to observe clinical course and evaluate the effect of possible drugs to treat myocarditis.

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