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The ultrastructural changes in the left ventricles of rabbits with alloxan (100 mg/kg i.v.)-induced diabetes were examined. Injection of alloxan resulted in a diabetic state characterized by increased hemoglobin glycosylation, blood and urine glucose and a significant depression of serum insulin levels. Electron microscopic examination of 10-week diabetic hearts revealed a spectrum of abnormalities ranging from mild to severe. Cardiac muscle cells in diabetic hearts showed some myofibrillar damage and varying degrees of contraction. The most prominent findings, however, were alterations in the mitochondria. Swollen and fragmented mitochondria containing amorphous dense bodies were evident upon electron microscopic examination. The cristae in the mitochondria appeared distorted and in some cases were completely lysed. A marked increase in lipid droplets and glycogen granules was also apparent. In addition, the sarcoplasmic reticulum was dilated and contained varying degrees of electron-dense material. These ultrastructural alterations suggest that the cardiomyopathy observed in alloxan-induced diabetic rabbits could be due to alterations in the vasculature or may be secondary to a number of metabolic alterations previously reported in this model.

Biochemical and myocardial functional changes were determined in rabbits made diabetic with alloxan (100 mg/kg, intravenously, two injections 24 h apart). Alloxan-induced diabetes was characterized by a state of hypoinsulinaemia and hyperglycaemia. After 10 weeks of diabetes, significant decreases in heart and left ventricular weights as well as increased serum and heart triglycerides and cholesterol were observed in the diabetic animals (p less than 0.05). In addition, left ventricular pressure, heart rate and rate of left ventricular pressure development were all decreased in the animals. The diabetic state was also associated with a slight elevation in myocardial calcium and a significant decrease in magnesium levels (p less than 0.05). Subcellular fractionation of diabetic hearts indicated the presence of alterations in myofibrillar and sarcoplasmic reticulum marker enzymes (p less than 0.05). Among the lysosomal enzymes, measured, N-acetyl-beta-glucosaminidase activity was significantly increased in the homogenates of diabetic left ventricles (p less than 0.05). These alterations in hearts of diabetic rabbits may be responsible for some aspects of diabetic cardiomyopathy.

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