Role of acetylstrophanthidin in augmenting myocardial oxygen consumption. Relation of increased O-2 consumption to changes in velocity of contraction.

A polarographic method was used to determine the effects of acetylstrophanthidin on myocardial oxygen consumption (MVO2) of 19 cat papillary muscles contracting under both afterloaded and isometric conditions. Under afterloaded conditions, acetylstrophanthidin shifted the force-velocity relation to the right and produced increments in both the extent and velocity of shortening at constant levels of developed force. These changes in myocardial mechanical behavior after strophanthidin were always associated with an increased MVO. Since both the extent and velocity of shortening increased following augmentation of the contractile state with glycoside, consideration of the individual effect of these variables in myocardial mechanical behavior on MVO was precluded. Therefore, experiments were performed on isometrically contracting muscle to evaluate the effect of changes in the velocity of contraction on MVO;> independent of changes in contractile element shortening. Comparison of the MVO2 of isometric contractions at equal levels of developed tension (and thus equivalent amounts of internal contractile element shortening) was accomplished by decreasing initial muscle length after augmentation of the contractile state by acetylstrophanthidin. Under these conditions, augmentation of the contractile state, characterized by an increase in the velocity of contraction, was associated with an increased MVO. Thus it is concluded that the effect of acetylstrophanthidin is to increase MVO2 at a constant load and that this augmentation of MVO2 can be related to the change in contractile state of the muscle. ADDITIONAL