WILLIAM GROSSMAN, M.D.; NOEL I. ROBIN, M.D.; LEWIS W. JOHNSON, M.D.; HAROLD L. BROOKS, M.D.; HERBERT A. SELENKOW, M.D., F.A.C.P.; LEWIS DEXTER, M.D., F.A.C.P.
The role of beta adrenergic influences in maintaining the enhanced myocardial contractility of thyrotoxicosis was studied in 10 hyperthyroid patients, using sotalol, a beta adrenergic blocking agent free of intrinsic myocardial depressant properties. The isovolumic contraction period, corrected ejection time, and the ratio of the pre-ejection period to the left ventricular ejection time were used as indexes of myocardial contractility and showed no significant change after beta receptor blockade with sotalol. Heart rate decreased (109 ± 6 beats/min to 83 ± 5 beats/min or -24%; P < 0.01), pulse pressure decreased (89 ± 14 mm Hg to 73 ± 10 mm Hg or -17%; P < 0.02), and circulation time (hand to tongue) increased (14.5 ± 1.5 sec to 17.3 ± 1.8 sec or +9%; P < 0.05) after beta blockade. No significant changes occurred in oxygen consumption, skin temperature, respiratory rate, or serum thyroxine. Although the tachycardia, shortened circulation time, and widened pulse pressure of thyrotoxicosis are apparently mediated by beta adrenergic influences, the heightened ventricular function associated with thyrotoxicosis seems to be independent of beta adrenergic influences and probably represents a primary effect of thyroxine on the heart.
GROSSMAN W, ROBIN NI, JOHNSON LW, et al. The Enhanced Myocardial Contractility of Thyrotoxicosis: Role of the Beta Adrenergic Receptor. Ann Intern Med. 1971;74:869–874. doi: 10.7326/0003-4819-74-6-869
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Published: Ann Intern Med. 1971;74(6):869-874.
Cardiology, Endocrine and Metabolism, Thyroid Disorders.
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