Hasin Y, Yarom A, Rogel S
J Electrocardiol. 1977;10(4):367-73. doi: 10.1016/s0022-0736(77)80010-1.
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.
在体搏动的犬心脏中研究了心房肌的兴奋性阈值。构建了单极阴极和阳极强度 - 间期曲线，发现它们的形状不同。发现在心房相对不应期内的任何间期，与心室一样，存在由刺激心房心肌的阈值上限（TU）和下限（TL）界定的广泛电流水平范围。在这些限度内，阈值自发变化，并且可以通过一连串早搏将其降低至TL水平。在给予治疗剂量的奎尼丁、普鲁卡因胺或利多卡因后，反复测定此类TU和TL曲线。观察到所有三种药物均延长了不应期。每种药物给药后，TU值均增加，奎尼丁给药后增加最多，而TL曲线受奎尼丁的影响较小。有人提出，由此产生的出口阻滞是奎尼丁抑制心房心律失常的主要机制。
