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Kazumasa Hiejima - One of the best experts on this subject based on the ideXlab platform.
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Atrioventricular nodal reentrant tachycardia with retrograde block induced by Aprindine
Journal of electrocardiology, 1992Co-Authors: Kaoru Okishige, Fumio Suzuki, Kazumasa Hiejima, K. Hirao, Humio Suzuki, Paul J. Wang, Peter L. FriedmanAbstract:Two patients are described who had atrioventricular nodal reentrant tachycardia (AVNRT) with 1:1 relationship in the control state, but in whom a varying degree of VA block during AVNRT was observed during therapy with Aprindine. Aprindine, however, did not cause anterograde blockade of conduction over the slow AV nodal pathway during tachycardia. These observations support the conclusion that the bulk of atrial muscle is not a requisite part of the tachycardia circuit in AVNRT and that antiarrhythmic drugs may have disparate effects on conduction in the retrograde and anterograde limbs of the circuit.
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Combination therapy with Aprindine and verapamil for paroxysmal supraventricular tachycardia as assessed by transesophageal atrial pacing
Cardiovascular Drugs and Therapy, 1991Co-Authors: Kenzo Hirao, Kaoru Okishige, Fumio Suzuki, Kazumasa HiejimaAbstract:To assess the efficacy of combination therapy of Aprindine (40 mg/day) and verapamil (160 mg/day), transesophageal programmed atrial stimulation was performed on 21 patients with paroxysmal supraventricular tachycardia (including 12 patients with atrioventricular nodal reentrant tachycardia and nine patients with atrioventricular reentrant tachycardia) under four conditions: a) control, b) Aprindine alone, c) verapamil alone, and d) Aprindine + verapamil. Results: a) Aprindine, verapamil, and Aprindine + verapamil prevented paroxysmal supraventricular tachycardia induction in 2/21, 3/21, and 9/21 patients, respectively;b) Aprindine + verapamil prolonged the cycle length of paroxysmal supraventricular tachycardia more than Aprindine or verapamil alone; c) Aprindine, verapamil, and Aprindine + verapamil decreased the AV blocking rate by 15, 23, and 35 beats/min, respectively, in comparison with the control state; d) Aprindine, verapamil, and Aprindine + verapamil prolonged the effective refractory period of atrioventricular conduction system by 20, 34, and 76 msec, respectively, compared with the control state. In conclusion, Aprindine + verapamil appear to be more effective than Aprindine or verapamil alone in preventing paroxysmal supraventricular tachycardia with nodal reentry, but there was less benefit in those without nodal reentry (Wolff-Parkinson-White group).
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Combination therapy with Aprindine and verapamil for paroxysmal supraventricular tachycardia as assessed by transesophageal atrial pacing.
Cardiovascular drugs and therapy, 1991Co-Authors: Kenzo Hirao, Kaoru Okishige, Fumio Suzuki, Kazumasa HiejimaAbstract:To assess the efficacy of combination therapy of Aprindine (40 mg/day) and verapamil (160 mg/day), transesophageal programmed atrial stimulation was performed on 21 patients with paroxysmal supraventricular tachycardia (including 12 patients with atrioventricular nodal reentrant tachycardia and nine patients with atrioventricular reentrant tachycardia) under four conditions: a) control, b) Aprindine alone, c) verapamil alone, and d) Aprindine + verapamil. a) Aprindine, verapamil, and Aprindine + verapamil prevented paroxysmal supraventricular tachycardia induction in 2/21, 3/21, and 9/21 patients, respectively; b) Aprindine + verapamil prolonged the cycle length of paroxysmal supraventricular tachycardia more than Aprindine or verapamil alone; c) Aprindine, verapamil, and Aprindine + verapamil decreased the AV blocking rate by 15, 23, and 35 beats/min, respectively, in comparison with the control state; d) Aprindine, verapamil, and Aprindine + verapamil prolonged the effective refractory period of atrioventricular conduction system by 20, 34, and 76 msec, respectively, compared with the control state. In conclusion, Aprindine + verapamil appear to be more effective than Aprindine or verapamil alone in preventing paroxysmal supraventricular tachycardia with nodal reentry, but there was less benefit in those without nodal reentry (Wolff-Parkinson-White group).
Hiroto Mashiba - One of the best experts on this subject based on the ideXlab platform.
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Aprindine blocks the sodium current in guinea-pig ventricular myocytes
Naunyn-Schmiedeberg's Archives of Pharmacology, 1991Co-Authors: Ryoichi Sato, Ichiro Hisatome, Yasunori Tanaka, Norito Sasaki, Hiroshi Kotake, Hiroto Mashiba, Ryo KatoriAbstract:Aprindine is a class Ib antiarrhythmic agent. We studied effects of Aprindine (3 µmol/l) on the Na^+ current using whole cell voltage clamp (tip resistance = 0.5 Ω, [Na]_i and_o = 10 mmol/l at 18°C). Aprindine revealed tonic block (Kd_rest = 37.7 µmol/l, Kd_i = 0.74 µmol/l; n = 4). Aprindine, shifted inactivation curve to hyperpolarizing direction by 11.4 ± 3.5 mV (n = 4) without changes in slope factor. In the presence of 3 µmol/l Aprindine, Aprindine showed phasic block, i.e., duration-dependent block at 2 Hz (64% ±3070 at 1.5 ms, 82%±6% at 20 ms, 93%±7% at 200 ms; n = 4). Short single prepulse also produced Aprindine-induced phasic block (12% at 1.5 ms, 22% at 100 ms; n = 2). After removal of fast inactivation of Na^+ current by 3 mmol/l tosylchloramide sodium, Aprindine revealed phasic block, independent of holding potential. The recovery time constant from Aprindine-induced phasic block was 4.8 s at holding potential = −100 mV and 5.0 s at holding potential = –140 mV. This use-dependent block of Aprindine had pH dependency. Under acidic condition (pH 6.0), 3 µmol/l Aprindine showed smaller use-dependent block (14% ± 7% at 2 Hz; n = 4) comparing with either at pH 7,4 (68% ± 13%; n = 4) or at pH 8.0 (90% ±12%; n = 4). The results suggest that Aprindine could bind to the receptor via activation process through channel pore, resulting in decrease of Na^+ current, and egress from the receptor through the lipid bilayer. These effects might be attenuated under acidic condition due to changes in intracellular ratio of charged to neutralized form of drug molecule.
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Aprindine blocks the sodium current in guinea-pig ventricular myocytes.
Naunyn-Schmiedeberg's archives of pharmacology, 1991Co-Authors: Ryoichi Sato, Ichiro Hisatome, Yasunori Tanaka, Hiroshi Kotake, Hiroto Mashiba, Sasaki N, Ryo KatoriAbstract:Aprindine is a class Ib antiarrhythmic agent. We studied effects of Aprindine (3 mumol/l) on the Na+ current using whole cell voltage clamp (tip resistance = 0.5 M omega, [Na]i ando = 10 mmol/l at 18 degrees C). Aprindine revealed tonic block (Kdrest = 37.7 mumol/l, Kdi = 0.74 mumol/l; n = 4). Aprindine, shifted inactivation curve to hyperpolarizing direction by 11.4 +/- 3.5 mV (n = 4) without changes in slope factor. In the presence of 3 mumol/l Aprindine, Aprindine showed phasic block, i.e., duration-dependent block at 2 Hz (64% +/- 3% at 1.5 ms, 82% +/- 6% at 20 ms, 93% +/- 7% at 200 ms; n = 4). Short single prepulse also produced Aprindine-induced phasic block (12% at 1.5 ms, 22% at 100 ms; n = 2). After removal of fast inactivation of Na+ current by 3 mmol/l tosylchloramide sodium, Aprindine revealed phasic block, independent of holding potential. The recovery time constant from Aprindine-induced phasic block was 4.8 s at holding potential = -100 mV and 5.0 s at holding potential = -140 mV. This use-dependent block of Aprindine had pH dependency. Under acidic condition (pH 6.0), 3 mumol/l Aprindine showed smaller use-dependent block (14% +/- 7% at 2 Hz; n = 4) comparing with either at pH 7.4 (68% +/- 13%; n = 4) or at pH 8.0 (90% +/- 12%; n = 4). The results suggest that Aprindine could bind to the receptor via activation process through channel pore, resulting in decrease of Na+ current, and egress from the receptor through the lipid bilayer. These effects might be attenuated under acidic condition due to changes in intracellular ratio of charged to neutralized form of drug molecule.
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Effects of Aprindine on conduction velocity and Vmax in guinea-pig papillary muscles.
Journal of clinical pharmacology, 1991Co-Authors: Shozo Hirai, Ichiro Hisatome, Hiroshi Kotake, Junichi Hasegawa, Yasutaka Kurata, Takahiro Nawada, Noriyasu Noguchi, Satoshi Matsuoka, Hiroto MashibaAbstract:One of the effects of antiarrhythmic drugs is the reduction of conduction velocity. Cable theory predicts that there is a nonlinear relationship between conduction velocity and upstroke velocity (Vmax) of action potential. By using conventional microelectrode techniques, Aprindine-induced reduction of Vmax of action potential and conduction velocity in guinea-pig papillary muscles were measured. Aprindine-produced, use-dependent, and concentration-dependent changes in conduction velocity and the decline of square of conduction velocity was well fit by a single exponential. Time constants for square of conduction velocity were comparable to simultaneously measured time constants for effects of Vmax. At a concentration of 1 to 10 microM Aprindine, onset changes between Vmax and conduction velocity had a log-linear relationship in a predicted fashion. Whereas, in the recovery process from Aprindine-induced depression, slow recovery time course of conduction velocity was observed. In conclusion, in the presence of Aprindine, only onset block of conduction velocity can be analyzed quantitatively in the relationship to observation on Vmax in vitro. These results suggested that in the presence of Aprindine, the recovery of internal conductance may be slower than that of Vmax.
Kenzo Hirao - One of the best experts on this subject based on the ideXlab platform.
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Combination therapy with Aprindine and verapamil for paroxysmal supraventricular tachycardia as assessed by transesophageal atrial pacing
Cardiovascular Drugs and Therapy, 1991Co-Authors: Kenzo Hirao, Kaoru Okishige, Fumio Suzuki, Kazumasa HiejimaAbstract:To assess the efficacy of combination therapy of Aprindine (40 mg/day) and verapamil (160 mg/day), transesophageal programmed atrial stimulation was performed on 21 patients with paroxysmal supraventricular tachycardia (including 12 patients with atrioventricular nodal reentrant tachycardia and nine patients with atrioventricular reentrant tachycardia) under four conditions: a) control, b) Aprindine alone, c) verapamil alone, and d) Aprindine + verapamil. Results: a) Aprindine, verapamil, and Aprindine + verapamil prevented paroxysmal supraventricular tachycardia induction in 2/21, 3/21, and 9/21 patients, respectively;b) Aprindine + verapamil prolonged the cycle length of paroxysmal supraventricular tachycardia more than Aprindine or verapamil alone; c) Aprindine, verapamil, and Aprindine + verapamil decreased the AV blocking rate by 15, 23, and 35 beats/min, respectively, in comparison with the control state; d) Aprindine, verapamil, and Aprindine + verapamil prolonged the effective refractory period of atrioventricular conduction system by 20, 34, and 76 msec, respectively, compared with the control state. In conclusion, Aprindine + verapamil appear to be more effective than Aprindine or verapamil alone in preventing paroxysmal supraventricular tachycardia with nodal reentry, but there was less benefit in those without nodal reentry (Wolff-Parkinson-White group).
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Combination therapy with Aprindine and verapamil for paroxysmal supraventricular tachycardia as assessed by transesophageal atrial pacing.
Cardiovascular drugs and therapy, 1991Co-Authors: Kenzo Hirao, Kaoru Okishige, Fumio Suzuki, Kazumasa HiejimaAbstract:To assess the efficacy of combination therapy of Aprindine (40 mg/day) and verapamil (160 mg/day), transesophageal programmed atrial stimulation was performed on 21 patients with paroxysmal supraventricular tachycardia (including 12 patients with atrioventricular nodal reentrant tachycardia and nine patients with atrioventricular reentrant tachycardia) under four conditions: a) control, b) Aprindine alone, c) verapamil alone, and d) Aprindine + verapamil. a) Aprindine, verapamil, and Aprindine + verapamil prevented paroxysmal supraventricular tachycardia induction in 2/21, 3/21, and 9/21 patients, respectively; b) Aprindine + verapamil prolonged the cycle length of paroxysmal supraventricular tachycardia more than Aprindine or verapamil alone; c) Aprindine, verapamil, and Aprindine + verapamil decreased the AV blocking rate by 15, 23, and 35 beats/min, respectively, in comparison with the control state; d) Aprindine, verapamil, and Aprindine + verapamil prolonged the effective refractory period of atrioventricular conduction system by 20, 34, and 76 msec, respectively, compared with the control state. In conclusion, Aprindine + verapamil appear to be more effective than Aprindine or verapamil alone in preventing paroxysmal supraventricular tachycardia with nodal reentry, but there was less benefit in those without nodal reentry (Wolff-Parkinson-White group).
Kaoru Okishige - One of the best experts on this subject based on the ideXlab platform.
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Atrioventricular nodal reentrant tachycardia with retrograde block induced by Aprindine
Journal of electrocardiology, 1992Co-Authors: Kaoru Okishige, Fumio Suzuki, Kazumasa Hiejima, K. Hirao, Humio Suzuki, Paul J. Wang, Peter L. FriedmanAbstract:Two patients are described who had atrioventricular nodal reentrant tachycardia (AVNRT) with 1:1 relationship in the control state, but in whom a varying degree of VA block during AVNRT was observed during therapy with Aprindine. Aprindine, however, did not cause anterograde blockade of conduction over the slow AV nodal pathway during tachycardia. These observations support the conclusion that the bulk of atrial muscle is not a requisite part of the tachycardia circuit in AVNRT and that antiarrhythmic drugs may have disparate effects on conduction in the retrograde and anterograde limbs of the circuit.
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Combination therapy with Aprindine and verapamil for paroxysmal supraventricular tachycardia as assessed by transesophageal atrial pacing
Cardiovascular Drugs and Therapy, 1991Co-Authors: Kenzo Hirao, Kaoru Okishige, Fumio Suzuki, Kazumasa HiejimaAbstract:To assess the efficacy of combination therapy of Aprindine (40 mg/day) and verapamil (160 mg/day), transesophageal programmed atrial stimulation was performed on 21 patients with paroxysmal supraventricular tachycardia (including 12 patients with atrioventricular nodal reentrant tachycardia and nine patients with atrioventricular reentrant tachycardia) under four conditions: a) control, b) Aprindine alone, c) verapamil alone, and d) Aprindine + verapamil. Results: a) Aprindine, verapamil, and Aprindine + verapamil prevented paroxysmal supraventricular tachycardia induction in 2/21, 3/21, and 9/21 patients, respectively;b) Aprindine + verapamil prolonged the cycle length of paroxysmal supraventricular tachycardia more than Aprindine or verapamil alone; c) Aprindine, verapamil, and Aprindine + verapamil decreased the AV blocking rate by 15, 23, and 35 beats/min, respectively, in comparison with the control state; d) Aprindine, verapamil, and Aprindine + verapamil prolonged the effective refractory period of atrioventricular conduction system by 20, 34, and 76 msec, respectively, compared with the control state. In conclusion, Aprindine + verapamil appear to be more effective than Aprindine or verapamil alone in preventing paroxysmal supraventricular tachycardia with nodal reentry, but there was less benefit in those without nodal reentry (Wolff-Parkinson-White group).
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Combination therapy with Aprindine and verapamil for paroxysmal supraventricular tachycardia as assessed by transesophageal atrial pacing.
Cardiovascular drugs and therapy, 1991Co-Authors: Kenzo Hirao, Kaoru Okishige, Fumio Suzuki, Kazumasa HiejimaAbstract:To assess the efficacy of combination therapy of Aprindine (40 mg/day) and verapamil (160 mg/day), transesophageal programmed atrial stimulation was performed on 21 patients with paroxysmal supraventricular tachycardia (including 12 patients with atrioventricular nodal reentrant tachycardia and nine patients with atrioventricular reentrant tachycardia) under four conditions: a) control, b) Aprindine alone, c) verapamil alone, and d) Aprindine + verapamil. a) Aprindine, verapamil, and Aprindine + verapamil prevented paroxysmal supraventricular tachycardia induction in 2/21, 3/21, and 9/21 patients, respectively; b) Aprindine + verapamil prolonged the cycle length of paroxysmal supraventricular tachycardia more than Aprindine or verapamil alone; c) Aprindine, verapamil, and Aprindine + verapamil decreased the AV blocking rate by 15, 23, and 35 beats/min, respectively, in comparison with the control state; d) Aprindine, verapamil, and Aprindine + verapamil prolonged the effective refractory period of atrioventricular conduction system by 20, 34, and 76 msec, respectively, compared with the control state. In conclusion, Aprindine + verapamil appear to be more effective than Aprindine or verapamil alone in preventing paroxysmal supraventricular tachycardia with nodal reentry, but there was less benefit in those without nodal reentry (Wolff-Parkinson-White group).
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Experimental study on the electrophysiological effects of the combination of the antiarrhythmic drugs Aprindine and verapamil.
Archives internationales de pharmacodynamie et de therapie, 1991Co-Authors: Kaoru Okishige, Ohtomo K, Satoh T, Hiejima KAbstract:The acute electrophysiological effects of the antiarrhythmic drugs Aprindine and verapamil, injected intravenously either alone or in combination, were studied in 14 dogs during invasive electrophysiology. The AH and HV intervals during sinus rhythm were significantly prolonged, especially in the Aprindine and the Aprindine plus verapamil groups. The cycle lengths of the antegrade and retrograde atrio-ventricular block were most prolonged in the combination group. The effective refractory period and the functional refractory period of the atrial tissue, as well as the functional refractory period of the atrio-ventricular node, the effective refractory period of ventricular tissue and the ventriculo-atrial conduction system were most prolonged when the combination of the agents was given. The effective refractory period of the atrio-ventricular node was prolonged in the groups receiving verapamil and verapamil plus Aprindine. There was no significant difference in the serum concentration of each agent given alone or in combination. These results suggest that the efficacy of the combination of verapamil and Aprindine may be due to additive or synergistic effects of these antiarrhythmic agents.
Ichiro Hisatome - One of the best experts on this subject based on the ideXlab platform.
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Aprindine blocks the sodium current in guinea-pig ventricular myocytes
Naunyn-Schmiedeberg's Archives of Pharmacology, 1991Co-Authors: Ryoichi Sato, Ichiro Hisatome, Yasunori Tanaka, Norito Sasaki, Hiroshi Kotake, Hiroto Mashiba, Ryo KatoriAbstract:Aprindine is a class Ib antiarrhythmic agent. We studied effects of Aprindine (3 µmol/l) on the Na^+ current using whole cell voltage clamp (tip resistance = 0.5 Ω, [Na]_i and_o = 10 mmol/l at 18°C). Aprindine revealed tonic block (Kd_rest = 37.7 µmol/l, Kd_i = 0.74 µmol/l; n = 4). Aprindine, shifted inactivation curve to hyperpolarizing direction by 11.4 ± 3.5 mV (n = 4) without changes in slope factor. In the presence of 3 µmol/l Aprindine, Aprindine showed phasic block, i.e., duration-dependent block at 2 Hz (64% ±3070 at 1.5 ms, 82%±6% at 20 ms, 93%±7% at 200 ms; n = 4). Short single prepulse also produced Aprindine-induced phasic block (12% at 1.5 ms, 22% at 100 ms; n = 2). After removal of fast inactivation of Na^+ current by 3 mmol/l tosylchloramide sodium, Aprindine revealed phasic block, independent of holding potential. The recovery time constant from Aprindine-induced phasic block was 4.8 s at holding potential = −100 mV and 5.0 s at holding potential = –140 mV. This use-dependent block of Aprindine had pH dependency. Under acidic condition (pH 6.0), 3 µmol/l Aprindine showed smaller use-dependent block (14% ± 7% at 2 Hz; n = 4) comparing with either at pH 7,4 (68% ± 13%; n = 4) or at pH 8.0 (90% ±12%; n = 4). The results suggest that Aprindine could bind to the receptor via activation process through channel pore, resulting in decrease of Na^+ current, and egress from the receptor through the lipid bilayer. These effects might be attenuated under acidic condition due to changes in intracellular ratio of charged to neutralized form of drug molecule.
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Aprindine blocks the sodium current in guinea-pig ventricular myocytes.
Naunyn-Schmiedeberg's archives of pharmacology, 1991Co-Authors: Ryoichi Sato, Ichiro Hisatome, Yasunori Tanaka, Hiroshi Kotake, Hiroto Mashiba, Sasaki N, Ryo KatoriAbstract:Aprindine is a class Ib antiarrhythmic agent. We studied effects of Aprindine (3 mumol/l) on the Na+ current using whole cell voltage clamp (tip resistance = 0.5 M omega, [Na]i ando = 10 mmol/l at 18 degrees C). Aprindine revealed tonic block (Kdrest = 37.7 mumol/l, Kdi = 0.74 mumol/l; n = 4). Aprindine, shifted inactivation curve to hyperpolarizing direction by 11.4 +/- 3.5 mV (n = 4) without changes in slope factor. In the presence of 3 mumol/l Aprindine, Aprindine showed phasic block, i.e., duration-dependent block at 2 Hz (64% +/- 3% at 1.5 ms, 82% +/- 6% at 20 ms, 93% +/- 7% at 200 ms; n = 4). Short single prepulse also produced Aprindine-induced phasic block (12% at 1.5 ms, 22% at 100 ms; n = 2). After removal of fast inactivation of Na+ current by 3 mmol/l tosylchloramide sodium, Aprindine revealed phasic block, independent of holding potential. The recovery time constant from Aprindine-induced phasic block was 4.8 s at holding potential = -100 mV and 5.0 s at holding potential = -140 mV. This use-dependent block of Aprindine had pH dependency. Under acidic condition (pH 6.0), 3 mumol/l Aprindine showed smaller use-dependent block (14% +/- 7% at 2 Hz; n = 4) comparing with either at pH 7.4 (68% +/- 13%; n = 4) or at pH 8.0 (90% +/- 12%; n = 4). The results suggest that Aprindine could bind to the receptor via activation process through channel pore, resulting in decrease of Na+ current, and egress from the receptor through the lipid bilayer. These effects might be attenuated under acidic condition due to changes in intracellular ratio of charged to neutralized form of drug molecule.
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Effects of Aprindine on conduction velocity and Vmax in guinea-pig papillary muscles.
Journal of clinical pharmacology, 1991Co-Authors: Shozo Hirai, Ichiro Hisatome, Hiroshi Kotake, Junichi Hasegawa, Yasutaka Kurata, Takahiro Nawada, Noriyasu Noguchi, Satoshi Matsuoka, Hiroto MashibaAbstract:One of the effects of antiarrhythmic drugs is the reduction of conduction velocity. Cable theory predicts that there is a nonlinear relationship between conduction velocity and upstroke velocity (Vmax) of action potential. By using conventional microelectrode techniques, Aprindine-induced reduction of Vmax of action potential and conduction velocity in guinea-pig papillary muscles were measured. Aprindine-produced, use-dependent, and concentration-dependent changes in conduction velocity and the decline of square of conduction velocity was well fit by a single exponential. Time constants for square of conduction velocity were comparable to simultaneously measured time constants for effects of Vmax. At a concentration of 1 to 10 microM Aprindine, onset changes between Vmax and conduction velocity had a log-linear relationship in a predicted fashion. Whereas, in the recovery process from Aprindine-induced depression, slow recovery time course of conduction velocity was observed. In conclusion, in the presence of Aprindine, only onset block of conduction velocity can be analyzed quantitatively in the relationship to observation on Vmax in vitro. These results suggested that in the presence of Aprindine, the recovery of internal conductance may be slower than that of Vmax.