1 Cardiology Branch, National Heart and Lung Institute, Bethesda, Maryland 20014, and the Department of Medicine, University of California at San Diego, La Jolla, California 92037
To clarify the effects of hyperthyroidism on myocardial oxygen consumption (VO2), a polarographic method was employed to compare the VO2 of isolated papillary muscles from 13 normal euthyroid cats with that of 11 hyperthyroid cats. Basal VO2 was greater in the hyperthyroid group (3.03±0.20 vs. 2.36±0.19 SE filter-ing dry wrr1 · hour1, P < 0.05). In muscles studied under afterloaded isotonic conditions, hyperthyroidism shifted the forcevelocity curve upward and to the right, with an increase in both extent and velocity of shortening at equivalent loads. These changes in myocardial behavior in hyperthyroidism were associated with an increase in myocardial VO2. Isometrically contracting muscles from hyperthyroid animals demonstrated significant increases in both developed tension (6.3±0.7 vs. 4.7±0.4 g/mm2, P < 0.05) and rate of tension development (32.6±3.5 vs. 19.4±1.5 g/mm2 · second-1, P < 0.01), as compared to the euthyroid group. Myocardial VO2, expressed per g/mm2 isometric developed tension, was significantly greater in the hyperthyroid group (0.641±0.09 vs. 0.42±0.04 milliter · mg dry wt-1 · beat-, P < 0.02). Thus, experimental hyperthyroidism augments myocardial VO2 whether measured in resting or contracting cardiac muscle. This increase can be attributed, at least in part, to $ie altered contractile function of the heart in hyperthyroidism.
Submitted on April 28, 1970
Accepted on July 20, 1970
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