In vivo atrial excitability and anti-arrhythmic drugs.
The threshold of excitability of the atrial muscle was studied in the in vivo beating canine heart. Unipolar cathodal and anodal strength-interval curves were constructed and found to be dissimilar in shape. It was found that at any interval within the relative refractory period of the atrium, as in the ventricle, there is a wide range of current levels delineated by an upper (TU) and lower (TL) limit of threshold which can stimulate the atrial myocardium. Within these limits the threshold varies spontaneously and can be reduced to TL level by a run of extrasystoles. Such TU and TL curves were repeatedly determined following administration of therapeutic doses of quinidine, procaine amide or lidocaine. It was observed that all three drugs prolonged the refractory period. The TU values increased following each of the drugs, and mostly after quinidine, while the TL curve was less affected by quinidine. It is suggested that the exit block thus produced is the principal mechanism whereby quinidine depresses atrial disrhythmias.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000188:drug therapy; D016275:Atrial Function; D004285:Dogs; D006325:Heart Atria / Q000187:drug effects; D006329:Heart Conduction System / Q000187:drug effects / Q000502:physiology*; D008012:Lidocaine / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D011342:Procainamide / Q000494:pharmacology; D011802:Quinidine / Q000494:pharmacology*
D008012:Lidocaine; D011802:Quinidine; D011342:Procainamide