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Research Article Free access | 10.1172/JCI106157
1Department of Medicine, Ohio State University College of Medicine, Columbus, Ohio 43210
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1Department of Medicine, Ohio State University College of Medicine, Columbus, Ohio 43210
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1Department of Medicine, Ohio State University College of Medicine, Columbus, Ohio 43210
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1Department of Medicine, Ohio State University College of Medicine, Columbus, Ohio 43210
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Published October 1, 1969 - More info
Anaerobically periused hearts from rats with experimentally induced hyperthyroidism exhibited accelerated deterioration of pacemaker activity and ventricular performance. The diminished anaerobic performance of hyperthyroid hearts was associated with decreased adenosine triphosphate (ATP) levels and a reduced rate of anaerobic glycolysis as reflected in decreased lactic acid production during 30 min of anoxic perfusion.
Studies on whole heart homogenates demonstrated inhibition at the phosphofructokinase (PFK) step of the glycolytic pathway. Such inhibition was not demonstrated in the hyperthyroid heart cytosol. It is postulated that an inhibitor of PFK which resides dominantly in the particulate fraction is probably responsible for the diminished anaerobic glycolysis and performance of the hyperthyroid heart.