Abstract
Veratrine, protoveratrine and andromedotoxin share the property, previously described for the cardiac glycosides, of depressing Purkinje conduction without depressing ventricular myocardial conduction in the dog heart-lung preparation.
Non-fibrillatory doses of protoveratrine and andromedotoxin increase the spontaneous A-V nodal rate of the heart and induce coupled idioventricular beats but leave intracardiac conduction relatively unimpaired.
Non-fibrillatory doses of veratrine, veratridine and cevadine delay the recovery of the several cardiac tissues but have little effect upon cardiac automaticity. This delay in recovery is manifested by marked prolongation of the refractory periods of auricle and ventricle, an increase in the frequency-sensitivity of A-A and A-V conduction, and alternation of conduction times of beats driven from auricle to ventricle and beats driven for longer distances along the right ventricle.
The relationship between these changes in the properties of the heart and the varieties of pre-fibrillatory arrhythmias induced by the agents is discussed.
Footnotes
- Received July 1, 1957.
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