Abstract
All chambers of the heart are affected in experimental cobalt cardiomyopathy, with atrial predilection. The primary morphological alteration is mitochondrial damage that possibly reflects an enzymatic block of oxidative decarboxylation at pyruvate and ketogluterate levels. In acute cobalt toxicity chelation of calcium may also be a contributory factor, resulting in deficient utilization of high-energy phosphates. Experimental cobalt cardiomyopathy requires preconditioning factors: protein deficiency appears to be one of them. Vegetative polypoid endocarditis is an important accompaniment in the model used, suggesting that in rats on a protein deficient diet cobalt produced endothelial damage in addition to a cardiocyte injury.
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