Effects of atrio-ventricular conduction of calcium-antagonistic coronary vasodilators, local anaesthetics and quinidine injected into the posterior and the anterior septal artery of the atrio-ventricular node preparation of the dog.
The effects on atrio-ventricular (A-V) conduction and blood flow of calcium-antagonists (verapamil, nifedipine and diltiazem), local anaesthetics (procaine and lidocaine) and quinidine were investigated in the isolated, cross-circulated A-V node preparation of the dog. The drugs were injected individually into the posterior septal artery (PSA) through which the upper part of the A-V node is mainly perfused or into the anterior septal artery (ASA) through which the lower part of the node and the more distal conduction system are perfused. Single injections into the PSA of nifedipine (0.3-10 mug), verapamil (1-30 mug), diltiazem (1-30 mug), quinidine (30-300 mug), lidocaine (100 mug-1 mg) and procaine (300 mug-3 mg) produced a dose-related increase in the A-V conduction time and with higher doses of these drugs a second or third degree block of A-V conduction occurred. Nifedipine (0.3-30 mug) and verapamil (1-100 mug) injected into the ASA scarcely affected A-V conduction. Quinidine (30 mug-1 mg) and lidocaine (100 mug-3 mg) injected into the ASA prolonged the A-V conduction time in a dose-related manner, although the effects were less prominent than those produced upon injection into the PSA. High doses of quinidine (3 mg) and lidocaine (3-10 mg) injected into the ASA altered the shape of ventricular bipolar electrograms and prolonged the time interval between an electrogram of the right bundle branch and that of the ventricle. The results are consistent with the hypothesis that in excitation of A-V nodal cells a slow calcium current rather than a fast sodium current plays an important role and that in the His-Purkinje-ventricular system the fast sodium current is predominant. Single injections of the 6 drugs into the PSA produced a dose-related increase in blood flow through the PSA. All drugs but nifedipine increased the blood flow in almost the same dose range that caused impairment of A-V conduction. Nifedipine was 10 times more potent in increasing the blood flow than in impairing A-V conduction.
D000200:Action Potentials / Q000187:drug effects; D000779:Anesthetics, Local / Q000494:pharmacology*; D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects*; D001552:Benzazepines / Q000494:pharmacology*; D002118:Calcium / Q000037:antagonists & inhibitors*; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects; D004110:Diltiazem / Q000494:pharmacology*; D004285:Dogs; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects*; D066298:In Vitro Techniques; D007267:Injections; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D009431:Neural Conduction / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D011343:Procaine / Q000494:pharmacology; D011802:Quinidine / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*; D014700:Verapamil / Q000494:pharmacology
D000779:Anesthetics, Local; D001552:Benzazepines; D014665:Vasodilator Agents; D011343:Procaine; D008012:Lidocaine; D014700:Verapamil; D004110:Diltiazem; D009543:Nifedipine; D011802:Quinidine; D002118:Calcium