Effects on atrial, AV nodal and ventricular ERP: Tedisamil caused a significant prolongation of A-ERP at 3 and 10 |J.M (control 36±2.9 ms, 3 |J.M 47.1±3.6 ms, 10 |J.M 58.3±4.4 ms, both P<0.05 versus control). This parameter was not influenced by D-sotalol at all concentrations used (control 36.4±3 ms, 10 |J.M 38.1±3.9 ms) (Figure 3). AV-ERP was slightly prolonged by both drugs. This prolongation only reached significance at 10 |J.M under the influence of D-sota-lol (control 105±1.9 ms, 10 |J.M 123±3.3 ms, P<0.01) (Figure 4).
Additionally, ERPs were determined at a cycle length of the conditioning stimuli at 200 and 180 ms, respectively. Tedisamil induced a significant prolongation of rate-dependent A-ERP at 3 and 10 |J.M (at 200 ms: control 37.1±2.9 ms, 10 |J.M 60±3.4 ms; at 180 ms: control 37.9±3.1 ms, 10 |J.M 58.3±4 ms), whereas this parameter remained unaffected by D-sotalol (Figure 3).

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

Figure 3 Effects of increasing concentrations of either tedisamil or D-sotalol on the atrial effective refractory period (A-ERP) at stimulation intervals of240, 200 and 180 ms

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

Figure 4 Effects of increasing concentrations of either tedisamil or D-sotalol on the atrioventricular nodal refractory period (AV-ERP) at stimulation intervals of240, 200 and 180 ms 
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