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Programmed Cell Death (Apoptosis) in the Myocardium with Acute Myocarditis.

Published online by Cambridge University Press:  02 July 2020

T. Nishikawa
Affiliation:
Department of Pathology, Tokyo Women's Medical College, Tokyo, 162Japan
S. Ishiyama
Affiliation:
Department of Pathology, Tokyo Women's Medical College, Tokyo, 162Japan
K. Takeda
Affiliation:
Department of Pathology, Tokyo Women's Medical College, Tokyo, 162Japan
T. Kasajima
Affiliation:
Department of Pathology, Tokyo Women's Medical College, Tokyo, 162Japan
S. Abe
Affiliation:
Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo,113,Japan
T. Shimojo
Affiliation:
Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo,113,Japan
H. Ito
Affiliation:
Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo,113,Japan
M. Hiroe
Affiliation:
Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo,113,Japan
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Extract

Acute myocarditis is a potentially lethal disease. However, the precise mechanism of myocardial damage in myocarditis is still unknown, although its pathogenesis seems to be involved in the result of natural killer cells, cytotoxic T cells and autoantibodies. Recently, it has been reported that programmed death of cardiac myocytes can be induced by several pathological conditions including infarction and end-stage cardiac failure. However, little is known about the myocardial cell death in myocarditis. In this study, we investigated whether myocardial cell death via apoptosis occurs in the heart tissue with myocarditis.

Since it has been reported that the pathogenesis of the tissue damage in viral myocarditis resembles that in experimental autoimmune myocarditis induced by myosin, we used an experimental model for autoimmune myocarditis induced in Lewis rat with the use of myosin as the antigen. Rats were sacrificed on days 14, 17 and 21 after myosin injection. The tissue specimens were taken from ventricle of the heart.

Type
Pathology
Copyright
Copyright © Microscopy Society of America 1997

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References

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5. This study was supported by Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture, Japan (No. 08670828), by a grant from the Japan Private School Promotion Foundation and by a grant from the Japan Research Promotion Society for Cardiovascular Disease.Google Scholar