Electron microscopic study of cardiac lesions induced in rats by isoproterenol and by repeated stress. With suggestion that idiopathic cardiomyopathy may be a "disease of adaptation".

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Abstract
An EM study of cardiac lesions induced in rats by isoproterenol and by repeated stress is described, and a possible pathogenetic mechanism of idiopathic cardiomyopathy is proposed. Three types of cardiac cells could be roughly differentiated according to the structure and arrangement of myofibrils: normo-type with normal structure and normal arrangement of myofibrils; nondestroyed-degenerated-type in which myofibrils show normal structure and abnormal arrangement; and destroyed-degenerated-type with destroyed myofibrils. Various degrees and frequency of mitochondrial changes (accumulation, variation of size, swelling, loss of cristae and myelin figure), increase of glycogen granules, dilatation of sarcoplasmic reticulum or T-tubules and nuclear changes were seen in every type. These 3 types seemed to correlate well with the degree of myocardial .beta.-adrenergic stimulation by isoproterenol or repeated stress. Normo-types were extensively observed in hearts exposed to mild myocardial .beta.-adrenergic stimulation. Nondestroyed-degenerated-types and destroyed-degenerated-types were frequently observed in hearts exposed to excessive myocardial .beta.-adrenergic stimulation. These rsults show a similarity between cardiac lesions induced in rats by isoproterenol or repeated stress and those seen in human idiopathic cardiomyopathy, and suggest the possibility that idiopathic cardiomyopathy is a disease of adaptation.