Basis for myocardial mechanical defects associated with non-insulin-dependent diabetes.
Basis for myocardial mechanical defects associated with non-insulin-dependent diabetes.
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DOI：
10.1152/ajpendo.1989.256.1.e25
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发表时间：
1989
期刊：
影响因子：
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通讯作者：
S. Schaffer;M. Mozaffari;M. Artman;G. Wilson
中科院分区：
文献类型：
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作者：
S. Schaffer;M. Mozaffari;M. Artman;G. Wilson
从12个月的非胰岛素依赖型糖尿病大鼠中分离的心脏表现出收缩和放松的速率降低。与收缩力异常相关的是肌球蛋白同工酶含量重新分布到最不活跃的V3形式。心肌松弛缺陷也与钙处理受损同时发生。糖尿病心脏组织总钙含量上升35%。与此同时，负责维持正常细胞质钙水平的泵的活性降低。游离钙浓度为2.0 μ m时，糖尿病心脏肌浆网状钙摄取率和腺苷三磷酸酶活性下降约30%。舒张期心室僵硬度显著增加。这些钙代谢异常的最终结果是糖尿病心脏机械性能的显著损害。
Hearts isolated from 12-mo non-insulin-dependent diabetic rats exhibited reduced rates of contractility and relaxation. Associated with the abnormality in contractility was a redistribution in myosin isozyme content to the least active V3 form. Defects in myocardial relaxation also occurred concomitantly with impaired handling of calcium. Total tissue calcium content rose 35% in the diabetic hearts. At the same time, the activity of the pump responsible for maintaining normal cytoplasmic calcium levels was reduced. At a free calcium concentration of 2.0 microM, the rates of sarcoplasmic reticular calcium uptake and adenosinetriphosphatase activity of the diabetic hearts were decreased approximately 30%. Diastolic ventricular stiffness increased dramatically. The net result of these abnormalities in calcium metabolism is a significant impairment in mechanical performance of the diabetic heart.