Key result
Cardiomyopathic hamsters exhibit marked myocyte hypertrophy alongside ~13% ventricular cell loss.
Why the study?
The study aimed to characterize size and shape differences of enzymatically isolated ventricular myocytes from rats and cardiomyopathic hamsters to understand cellular hypertrophy and contractility defects.
Rodent myocyte dimensions provide reference values; leaves open translation to human cardiomyopathy remodeling.
Rod-shaped and branched ventricular myocytes from rats and cardiomyopathic hamsters (strain 53.58) were isolated enzymatically, and their widths and lengths were measured in physiological salt solutions containing normal levels of calcium (2.5 mmol). In rats of approximately 200 g body weight, the average myocyte width and length are 25 micron and 115 micron. The isolated cells are also classified according to shape with nearly 50% branched or otherwise irregular. Myocytes of the hearts of the 53.58 strain of cardiomyopathic hamsters at 7 months of age are significantly larger than control hamsters of the same age, indicating that cellular hypertrophy has occurred. Estimates of the number of cells in the ventricles indicate that there is a cell loss of nearly 13% in the myopathic heart. A consideration of the significance of wider and longer myocytes with undiminished myofibrillar mass lead to the conclusion that the decreased contractility displayed by the cardiomyopathic hamster heart must be due, at least in part, to functional defects in the myofibrillar apparatus, in the system of activation, or in cellular integration.
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Sorenson et al. (1985) studied Cardiomyopathy. Cardiomyopathy (strain 53.58) vs. Control hamsters of the same age was evaluated on Myocyte size (width and length) and cell count. Ventricular myocytes from 7-month-old cardiomyopathic hamsters are significantly larger than those from controls, with an estimated ventricular cell loss of nearly 13% in the myopathic heart.
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