Modification of atrioventricular conduction under the combined influence of a cardiac glycoside and a calcium antagonist in the dog.
Conduction disorders may be logically expected from the digoxin-verapamil association, since each of these drugs is known to increase conduction time (CT) and effective refractory period (ERP) in the atrioventricular (AV) node. When AV conduction is considerably depressed by verapamil (1.27 mg/kg over 90 min) in the absence of vagal tone, digoxin, infused at 1 microgram/kg/min rate over 40 min, elicits a progressive but incomplete regression of the verapamil effects, as does hypercalcaemia up to 5.5 mmol/l. Infused at the 2.5 microgram/kg/min rate over 20 min, its antagonistic effects, like those of hypercalcaemia exceeding 5.5 mmol/l, are less and less marked and even replaced by a certain synergism. When AV conduction is considerably depressed by digoxin (i.v. injection of 40 micrograms/kg) under high vagal tone, verapamil (twice 0.2 mg/kg) does not aggravate this depression and even attenuates it, this attenuation being however more significant on ERP than CT in the AV node. Consequently, as a rule, the interaction does not lead to block, since the maximum action of one drug is associated with the reduction in the action of the other or even the conversion of synergism into antagonism.
D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects*; D002118:Calcium / Q000494:pharmacology; D004077:Digoxin / Q000494:pharmacology*; D004285:Dogs; D004347:Drug Interactions; D004558:Electric Stimulation; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D014630:Vagus Nerve / Q000502:physiology; D014700:Verapamil / Q000494:pharmacology*
D004077:Digoxin; D014700:Verapamil; D002118:Calcium