Suppression of ventricular automaticity by antidysrhythmic agents.
In view of the potentially important role of automaticity in the genesis of ventricular dysrhythmias, the effects of four widely used antidysrhythmic agents on ventricular automaticity were examined in anesthetized dogs at doses previously shown to antagonize experiments induced rhythm disturbances. Quinidine, and particularly procainamide, lidocaine and propranolol slowed ventricular rate in A-V blocked dogs. Quinidine and procainamide but particularly the last two agents also markedly prolonged overdrive suppression. Thus, all four substances depressed automaticity. However, propranolol was effective at doses substantially lower than those required to antagonize several experimental dysrhythmias.
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D003864:Depression, Chemical; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D011342:Procainamide / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011802:Quinidine / Q000494:pharmacology; D016276:Ventricular Function
D000889:Anti-Arrhythmia Agents; D008012:Lidocaine; D011433:Propranolol; D011802:Quinidine; D011342:Procainamide