Abstract
Ouabain-induced changes in cardiac contractile force and differences in the amount of ouabain required to induce arrhythmias and to produce death were evaluated in normal, thyroidectomized and thyroxine-treated dogs. It was found, that ouabain, following alterations in thyroid function, still substantially augmented cardiac contractile force in anesthetized open-chest dogs. In both the hypothyroid and the hyperthyroid animals a moderate dose of ouabain produced an increase in contractile force of approximately the same extent as in the euthyroid animals, although of slower onset in the hypothyroid dogs. Larger doses of ouabain caused a smaller positive inotropic response. in hyperthyroid dogs than in euthyroid and hypothyroid animals. Changes in thyroid function increased the arrhythmia-producing and the lethal dose of ouabain, which in the hyperthyroid dogs may have been due to the markedly elevated heart rate.
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