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. 1976 Nov-Dec;71(6):624-44.
doi: 10.1007/BF01906408.

Experimental hypothyroidism: depression of myocardial contractile function and hemodynamics and their reversibility by substitution with thyroid hormones

Experimental hypothyroidism: depression of myocardial contractile function and hemodynamics and their reversibility by substitution with thyroid hormones

B E Strauer et al. Basic Res Cardiol. 1976 Nov-Dec.

Abstract

Hemodynamics and myocardial muscle mechanics have been studied in 22 euthyroid and 60 hypothyroid cats in which experimental hypothyroidism has been produced by thyroidectomy 61 days prior to the examination. Left ventricular to body weight ratio was altered due to a decrease in left ventricular weight and an increase in body weight. Heart rate, cardiac output and cardiac index were decreased (by 12-15 per cent), whereas stroke volume remained unchanges. Peak systolic pressure of the left ventricle was moderately decreased, the other pressures were in the normal range. There was a marked and significant reduction of isovolumic contractility indices indicating a depression of myocardial contractility in situ by 20-27 per cent. The isolated ventricular myocardium exhibited decreases of isotonic muscle shortening, of maximum isometric tension development and of the rates of both, isotonic shortening and isometric tension development by 12-35 per cent. Force-velocity relationships of contraction and relaxation were depressed to lower values of contraction and relaxation velocity as well as of maximum isometric muscle tension. The alterations in myocardial muscle mechanics and hemodynamics were completely reversible following substitution of the hypothyroid group with physiological doses of L-thyroxine (5 mug/kg/day for 8-18 days). Excess increases of parameters of myocardial performance were found following substitution of the hypothyroid group with L-thyroxine (500 mug/kg/day) in accordance with the induction of experimental hyperthyroidism in these animals. The results demonstrate impaired myocardial contractility and hemodynamics in experimental hypothyroidism. These changes are completely reversible by substitution with L-thyroxine in accordance with a reversible thyroid cardiomyopathy. The cellular mechanisms responsible for the altered cardiac activity in experimental hypothyroidism are discussed.

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