Abstract
The effects of several concentrations of acetylstrophanthidin on the force of isometric contraction of isolated atrial and papillary muscle preparations obtained from cats, rats, guinea pigs and rabbits were determined at 15 different frequencies of contraction. Qualitatively similar results were obtained in all species. In strips of cat atrium it was possible to make a detailed analysis of the effect of acetyl-strophanthidin on the determinants of the relationship between the strength of contraction and the interval between contractions.
The positive inotropic effect of cardiac glycosides results at least in large part from the increase in the strength of the rested-state contraction. No significant effect on the production or the disappearance of the positive inotropic effect of activation (PIEA) was found. The decay of the negative inotropic effect of activation (NIEA) is apparently greatly accelerated in the presence of cardiac glycosides, but this may also be a reflection of their action on the state determining the strength of the rested-state contraction. Contraction of the muscle is not essential for the appearance of the altered state of the muscle which is produced by the cardiac glycosides and results in increased contractility. The positive inotropic effect of cardiac glycosides persists as long as the drug is present, even in the absence of activity.
The magnitude of the increase in the force of contraction produced by optimal concentrations of acetyl-strophanthidin is largely dependent on the strength of contraction in the absence of the drug. The greatest increase in the force of contraction is generally obtained at the lowest point on the interval-force curve, which occurs at widely different intervals in different species and regions of the heart. The increase in force is usually greater in hypodynamic muscle than in fresh muscle. These findings are consistent with the existence of a limit beyond which the force of contraction cannot be raised by cardiac glycosides.
Footnotes
- Received January 26, 1962.
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