期刊
JAPANESE HEART JOURNAL
卷 44, 期 1, 页码 111-126出版社
JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED
DOI: 10.1536/jhj.44.111
关键词
capillarization; diffusion distance of oxygen; fibrosis; neovascularization; heart failure; microcirculation; microangiography using synchrotron radiation
The cardiomyopathic hamster (BIO TO2) is a well-established model of heart failure. Deterioration of cardiac function in BIO TO2 is attributed to a defect in delta-sarcoglycan, whereas cardiac dysfunction in delta-sarcoglycan knockout mice is caused by microvascular abnormalities. We examined the relation between cardiac function and the microvasculature, including angiogenic factors, in BIO TO2. Methods and Results: At the age of 5 weeks, percent fractional shortening (%FS) and positive rate of change in left ventricular pressure over time (dP/dt max) were lower in BIO TO2 than in age-matched F I B controls. Capillary density, capillary/myocyte (CM) ratio, capillary domain area (CDA), and myocyte density were similar between BIO TO2 and FIB controls. At the ages of 13 and 20 weeks, BIO had significantly lower capillary and myocyte densities and a significantly higher CM ratio and CDA. Myocyte density positively correlated with %FS and dP/dt max. There were no significant differences in mRNA expression for VEGF, Flt-1, angiopoietin-1, or angiopoietin-2 between BIO TO2 and F I B control. Conclusion: Progressive myocyte loss is responsible for deterioration of cardiac function in BIO TO2. The impaired neovascularization may be involved in the progress of cardiac remodeling in cardiomyopathic hamsters.
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