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The contractile and electrical activity of papillary muscles from hypertrophied right ventricles of cats with artificial stenosis of the pulmonary artery was investigated. Contractility was considerably decreased along the entire force-velocity relationship, whereas no measurable alterations could be detected in the electrical activities as recorded by intracellular microelectrodes. By supramaximal Ca 2+ activation, the contractility of both the hypertrophied and the normal control preparations was increased to about the same final value. These findings are consistent with the concept that a disorder in the mechanism of excitation-contraction coupling underlies the depressed contractile state of hypertrophied cardiac muscle. In addition, it could be shown that the increase in volume of each cellular unit is clearly related to the decrease in contractility. This can tentatively be explained by the following assumptions. If the amount of Ca 2+ entering the cell per unit area is not changed in hypertrophy, then in a cell of increased diameter, the amount of Ca 2+ distributed per unit cell volume will be diminished. Since the excitation-contraction coupling of the heart is very sensitive to Ca 2+ , this Ca 2+ deficit should be reflected in a depression of contractility.
Kaufmann et al. (Mon,) studied this question.