At stimulation intervals of 200 and 180 ms, 1 and 3 |XM tedisamil did not prolong V-ERP. Only 10 |J.M tedisamil prolonged V-ERP at a stimulation cycle length of 200 ms (control 97±3.1 ms, 10 |J.M 112±7.9 ms, P<0.05) and at 180 ms (control 90±2.5 ms, 10 |J.M 111±9.0 ms, not significant). D-sotalol 10 |J.M induced at a stimulation rate of 200 ms a significant prolongation of the V-ERP (control 98±3.9 ms, 10 |J.M 115±6.1 ms, P<0.01), whereas the effect was attenuated at 180 ms (control 99±3.4 ms, 10 |J.M 109±6.2 ms, not significant) (Figure 5).
Sinus node recovery time: Sinus node recovery time remained nearly unaffected by both drugs at all concentrations, with the exception of 10 |J.M tedisamil, which induced a slight but significant prolongation (control 272±14 ms, 10 |J.M 405±27 ms, P<0.01).   Tedisamil only slightly prolonged V-ERP at all concentrations used, but at 10 |J.M this effect reached significance. D-sotalol 1 and 3 |J.M had a minor effect on this parameter, but it significantly prolonged V-ERP at 10 |jM (control 101±3.5 ms, 10 |J.M 119±5.2 ms, P<0.01) (Figure 5).

Cardiac electrophysiological effects of two class III antiarrhythmic agents, tedisamil and D-sotalol

Figure 5 Effects of increasing concentrations of either tedisamil or D-sotalol on the ventricular effective refractory period (V-ERP) at stimulation intervals of240, 200 and 180 ms
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