Electrophysiologic properties of a narrow isthmus in rabbit atrial tissue: cycle length dependent effect of quinidine.

The modulation of quinidine's effect by pacing cycle lengths was assessed over an isthmus of atrial myocardium, simulating the Wolff-Parkinson-White syndrome. Isolated rabbit atria were dissected so that two tissue blocks, A and B, were linked by an isthmus, 1 mm in width. Effective refractory period in the tissue blocks and over the isthmus was measured at cycle lengths of 1,000, 600, and 400 ms, and the minimum cycle length to sustain 1:1 conduction over the isthmus was measured before treatment, during quinidine superfusion (4 mg/L), and after washout. Longitudinal velocity over the isthmus was also measured. The increment in the effective refractory period in the tissue blocks by quinidine appeared to be similar, about 10% at three pacing cycle lengths (p > 0.05). However, the increment of the effective refractory period over the isthmus was modulated by pacing cycle lengths: greater increase at shorter cycle lengths (p < 0.001). Quinidine prolonged the minimum cycle length over the isthmus by 44 +/- 17%. Regression analysis showed that after quinidine there was a correlationship between conduction velocity and refractoriness over the isthmus (R = 0.85, p < 0.001). Intracellular implements showed stable action potentials, confirming the integrity of the preparation. We conclude that (i) quinidine preferentially prolongs refractoriness over the isthmus and (ii) quinidine's effect on refractoriness over the isthmus is cycle length dependent.