The effect of procaine amide on excitability, refractoriness and conduction in the mammalian heart.

1. Procaine amide completely protected the dog heart in situ against electrical induction of auricular fibrillation. It also produced a marked rise in the threshold for multiple firing and fibrillation in the ventricle. 2. It elevated thresholds to stimulation in both the auricle and the ventricle and depressed conduction in all parts of the heart. These changes varied with the plasma level of the drug. 3. In all experiments performed the absolute, relative and total refractory periods of the auricle, but not of the ventricle, were significantly prolonged. 4. The evidence now available suggests that the anti-arrhythmic action of procaine amide resides principally in its ability to depress the excitability of the heart rather than in its ability to prolong refractoriness.