Sorenson A L, Tepper D, Sonnenblick E H, Robinson T F, Capasso J M
Cardiovasc Res. 1985 Dec;19(12):793-9. doi: 10.1093/cvr/19.12.793.
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.
采用酶解法分离大鼠和心肌病仓鼠（53.58品系）的杆状和分支状心室肌细胞，并在含有正常钙水平（2.5 mmol）的生理盐溶液中测量其宽度和长度。在体重约200 g的大鼠中，平均肌细胞宽度和长度分别为25微米和115微米。分离出的细胞也根据形状进行分类，近50%为分支状或其他不规则形状。7月龄的53.58品系心肌病仓鼠心脏的肌细胞明显大于同龄对照仓鼠，表明发生了细胞肥大。对心室细胞数量的估计表明，病变心脏中细胞损失近13%。考虑到肌原纤维质量未减少但更宽更长的肌细胞的意义，得出的结论是，心肌病仓鼠心脏表现出的收缩力下降至少部分归因于肌原纤维装置、激活系统或细胞整合中的功能缺陷。
