Influence of Reserpine and βTM 10 on Digitalis-Induced Ventricular Arrhythmia
After catecholamine depletion by reserpine, the capacity of the digitalis materials to induce ventricular arrhythmia is diminished. In papillary muscles from cats pretreated with reserpine, the incidence of ouabain-induced extra beats is reduced. The dose of ac. stroph. necessary to induce ventricular arrhythmia in combination with vagal stimulation is increased by reserpine pretreatment. Threshold doses comparable to those in cats not pretreated with reserpine produced arrhythmia after the catecholamine stores were repleted with norepinephrine or isoproterenol.
In dogs with A-V block, βTM 10, an agent which prevents the release of catecholamines, markedly reduces the response of the ventricular pacemaker to ac. stroph.
Since the arrhythmias induced by large doses of ac. stroph. are not affected by reserpine pretreatment, it is concluded that while catecholamine release is the primary mechanism involved in the arrhythmia produced by small doses, another mechanism also plays a role in this action after larger doses.
Only in the dose of 10 mg/kg did it appear that catecholamine depletion did not account entirely for the action of reserpine. The ac. stroph. threshold dose was not increased to the same degree as with the smaller doses of reserpine, and the incidence of ventricular fibrillation induced by the large dose of ac. stroph was reduced.
Hypotension produced by reserpine and βTM 10 did not seem to be an important factor in depression of the responsiveness of the ventricular pacemaker to ac. stroph.
While the incidence of ouabain-induced extra beats was reduced by reserpine pretreatment, the action of ouabain to increase the tension developed by isolated papillary muscles was not affected.
- Received March 8, 1963.
- © 1963 American Heart Association, Inc.