Abstract
Alterations by reserpine of cardiac responses to ouabain, as well as the effect of reserpine pretreatment on acetylstrophanthidin-induced changes in myocardial potassium flux, have been investigated in the dog.
Reserpine pretreatment provided protection against ouabain-induced cardiac arrhythmias. This antiarrhythmic property appears to be at least partially independent of catecholamine depletion. Such depletion, however, may enhance the protective action of reserpine to the extent that it removes the centrally mediated component of digitalis arrhythmias.
Reserpine, given simultaneously with ouabain, facilitates toxicity. This facilitation appears best explained by the combined action of ouabain and released catecholamines to increase ventricular automaticity.
Catecholamine-depleting dose schedules of reserpine failed to reduce the positive inotropic response of onabain. It is concluded that the inotropic action of ouabain does not depend directly upon myocardial catecholamine stores.
Reserpine pretreatment did not alter the effects of acetylstrophanthidin on net myocardial potassium flux.
Footnotes
- Accepted December 21, 1964.
- The Williams & Wilkins Comapny
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