Changes in Cell Morphology, [Ca2+]i and pHi During Metabolic Inhibition in Isolated Myocytes of Diabetic Rats Using Dual-Loading of Fura-2 and BCECF
Diabetes Mellitus (DM) has been shown to be associated with heart failure in the absence of atherosclerosis (1,2), suggesting a diabetic cardiomyopathy (3,4). The mechanism of heart failure due to the diabetic cardiomyopathy remains to be elucidated. The small vessel disease (5) and the abnormalities of subcellular mechanisms such as myosin ATPase (6) and myosin isoenzymes (7), have been reported in DM myocardium. Recently, abnormalities of Ca2+ metabolism have been reported in DM myocardium, which showed decreased Ca2+-ATPase of sarcoplasmic reticulum (SR) (8,9) and sarcolemma (10). It has also been reported that the activity of Na+/Ca2+-exchange was lower in DM myocardium (11). Previous reports have suggested the possibility of the Ca2+ overload in diabetic cardiomyopathy (11).
KeywordsMetabolic Inhibition Diabetic Cardiomyopathy Diabetes Mellitus Group Sodium Cyanide Myosin Isoenzyme
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