Role of alpha 1-adrenergic receptors and the effect of bunazosin on the histopathology of cardiomyopathic Syrian hamsters of strain BIO 14.6
In order to clarify the pathological involvement of the sympathetic nervous system in the development of cardiomyopathy, a receptor-binding study was carried out on cardiomyopathic Syrian hamsters of strain BIO 14.6 (BIO) at 21 days (prenecrotic stage); 35-42 days (onset of cardiomyopathy); and 70-8...
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Published in | Japanese circulation journal Vol. 52; no. 2; pp. 181 - 187 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Japan
01.02.1988
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Subjects | |
Online Access | Get full text |
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Summary: | In order to clarify the pathological involvement of the sympathetic nervous system in the development of cardiomyopathy, a receptor-binding study was carried out on cardiomyopathic Syrian hamsters of strain BIO 14.6 (BIO) at 21 days (prenecrotic stage); 35-42 days (onset of cardiomyopathy); and 70-84 days of life (early cardiac hypertrophy). The newly developed alpha 1-blocker (bunazosin hydrochloride) was initially administered at doses of 100 micrograms/kg or 10 mg/kg to BIO hamsters at 21 days of life and continued for 70 days. At the onset of cardiomyopathy and early cardiac hypertrophy, there was an increase in the number of alpha 1-receptors in the BIO hamsters compared to controls, but there were no significant changes at the prenecrotic stage. On histopathological examination, 10 mg/kg bunazosin had a significant beneficial effect on cardiomyopathy [area of necrosis 1.38% in untreated vs 0.33% in treated animals; area of calcification 2.70% (untreated) vs 0.60% (treated); area of all myocardial injuries 6.97% (untreated) vs 3.19% (treated)]. However, 100 micrograms/kg bunazosin had no effect. It was concluded that the increase in the number of alpha 1-receptors may not be involved in the pathogenesis of cardiomyopathy but that alpha 1-receptors could be implicated in the later progression of the condition. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0047-1828 |
DOI: | 10.1253/jcj.52.181 |