[Studies on the effect of propranolol on heart mechanics and contractility in experimentally induced hyperthyroidism].
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Biomedical subjects
Publications and source records attributed to A Scherpe.
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The effect of propranolol on cardiac mechanics and haemodynamics was examined on isolated papillary muscle as well as in situ in the closed thorax in euthyroid and hyperthyroid cats. Under propranolol there occurred on isolated papillary muscle significant decreases of muscle contraction, contraction velocity, isometric tension rise velocity and load and velocity values of simultaneously determined force-velocity relations. The 50% decrease of the values found was demonstrable at ca. 5--8 mu/ml for euthyroidal muscles, at 0.3--0.5 mug/ml for hyperthyroidal muscles. Contractility indices determined in situ (dp/dtmax, VCEmax, extrapolated Vmax) showed in hyperthyroidism at equal propranolol concentration a decrease about twice as great as in euthyroidism. The findings, showing a raised responsiveness of the ventricular myocardium in experimental hyperthyroidism to the negative inotropic effect of propranolol are discussed with regard to the therapeutic use of propranolol in hyperthyroidism.
Myocardial mechanics and oxygen consumption were studied in right ventricular papillary muscles taken from cats pretreated with cristalline L-thyroxine (1 mg/kg/day, i.p.) 8-18 days prior to the examination. Isotonic afterloaded and isometric contractions were employed. Oxygen consumption was determined polarographically. Data obtained were compared with control studies on papillary muscles taken from euthyroid cats. In isotonic afterloaded contractions the extent of shortening was nearly identical in both groups. However, maximum rate of isometric tension development and velocity of isotonic shortening were considerably increased in hyperthyroid myocardium. Myocardial oxygen consumption was significantly increased in hyperthyroidism, primarily due to an increased maximum rate of isometric tension development and-to a lesser extent-to increased isotonic contraction velocity. In isometric contractions maximum tension development (preload near Lmax) was similar in both groups. However, maximum rate of isometric tension development was markedly increased in hyperthyroidism. A close and linear relationship was found between maximum rate of isometric tension development (isometric contraction) and myocardial oxygen consumption. The results demonstrate increases of velocity factors of myocardial performance in experimental hyperthyroidism. Myocardial oxygen consumption is significantly increased. This increase in oxygen consumption quantitatively has its mechanical equivalent in increased isometric contraction velocity and, to a small amount, in increased isotonic contraction velocity.
The influence of experimental hyperthyroidism (intraperitoneal injection of crystalline L-thyroxine 1 mg/kg/day, 8-18 days) on cardiac mechanics in contractility in situ were studied in 30 hyperthyroid cats and compared with an euthyroid control group (n equals 30). 1. In hyperthyroidism left ventricular weight was considerably increased. Hypertrophy in hyperthyroidism represents a special case of myocardial hypertrophy, associated with an increase of myocardial performance. 2. Heart rate, systolic pressure, cardiac index, external cardiac work and tension time index were increased by 60-180 per cent. 3. Indices of contractility (dp/dtmax, t-dp/dtmax, dp/dtmax/IP) as well as isovolumetric force velocity relationships and VCE-max and Vmax demonstrated a considerable increase of contractility. Maximum rate isovolumetric pressure fall was increased by 120 per cent. Experimental hyperthyroidism is characterized by hypercirculation associated with increases of pressure, volume and velocity factors. The results are discussed with regards to the effects of increased cardiac mechanics on myocardial energy balance.
The effect of experimental hyperthyroidism on myocardial mechanics was examined on isolated ventricular myocardium (right ventricular papillary muscle) of cats. 1. Isotonic muscle contraction and isometric tension development were largely unchanged compared with euthyroidism. 2. Isotonic contraction velocity and maximal isometric tension rise velocity showed considerable rises of between 41 and 78%. 3. Force-velocity relations of contraction showed changes with increases of contraction velocity with every degree of load. 4. Force-velocity relations of isotonic relaxation showed increases of isotonic relaxation maxima with comparable loads without any alteration of the typical course of the relaxation curves compared with euthyroidism. 5. Lowering the temperature (from 34 to 24 degrees C) produced a considerable fall of the raised contraction and relaxation velocity in hyperthyroidism whereas the values of muscle contraction and tension development important for the pump function were largely unchanged. It is concluded that the myocardium in experimental hyperthyroidism is characterised by a primarily velocity-related increase of inotropy. Lowering the temperature produces an effective fall of the raised velocity values. The mechanisms of the increase of inotropy and significance of the findings are discussed.