SUMMARY The role of calcium in the pathogenesis of hypertrophic cardiomyopathy was investigated experimentally. For this purpose the calcium antagonist verapamil and the calcium ionophore A23187 were administered to pregnant rats together with triac in order to observe their effect on triac induced myocardial disarray and hypertrophy in developing rat hearts. At a low dose verapamil reduced both the level of disarray and hypertrophy, but a higher dose produced hypertrophy when given alone. A23187 did not appreciably potentiate the actions of triac when given in combination but when administered alone produced both disarray and hypertrophy. Verapamil prevents the inward movement of calcium ions to the myocardial cell, whereas A23187 increases the inflow of calcium ions. The results suggest that the actions of triac in producing myocardial disarray and hypertrophy are attributable to an increased concentration of intracellular calcium.Hypertrophic cardiomyopathy, in common with all other cardiomyopathies, is of unknown aetiology.' It has been established that myofibrillar disarray is characteristic of hypertrophic cardiomyopathy,2 and it is likely that other cardiac muscle abnormalities, which permit firm morphological diagnosis,3 develop subsequently. Quantifiable ultrastructural changes, mimicking those seen in patients with hypertrophic cardiomyopathy, can be produced in the heart muscle of developing rats by administering triiodothyroacetic acid during pregnancy.4 This model, which was developed from observations that hypertrophic cardiomyopathy. can be associated with covert or overt hyperthyroidism,56 has been used to show that the deleterious effect of triac is due to an increase in cell membrane permeability.7 This study therefore suggested that an increased entry of calcium into the myocardial cells may be at least Requests for reprints to Dr E G J Olsen,
Severe cardiac hypertrophy has been produced experimentally in rats by long-term, low-dose treatment with tri-iodothyroacetic acid. The dose used was insufficient to cause any apparent systemic or metabolic effect. It is suggested that similar iodinated substances in the blood in man, resulting from normal or abnormal thyroid hormone catabolism, may be causally related to some forms of cardiomyopathy.
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