Masse C, Cazes M, Sassine A
Arch Int Pharmacodyn Ther. 1984 Jun;269(2):219-35.
The mechanisms of action of cibenzoline upon the electrical activity of the cardiac membrane in vitro, were studied using frog auricular preparations. Action potentials and transmembrane currents were examined using the double sucrose gap technique. Cibenzoline 2.6 X 10(-6) M reduced the amplitude and rate of depolarization of the action potential, slightly prolonged its duration and increased the refractory period. Voltage clamp analysis revealed a notable decrease in the amplitude of sodium rapid inward current, accompanied by a decrease in the kinetics of activation and inactivation, time to peak of the current was increased, as was the inactivation time constant. Cibenzoline delayed recovery from inactivation, reactivation time constants were increased. Cibenzoline also reduced the slow kinetic current due to calcium and sodium ions. The calcium portion of this current was less affected. These data lead to the conclusion that cibenzoline has the characteristics of class I and some class IV anti-arrhythmic action, but cibenzoline is not another quinidine because it would not appear to influence outward potassium current.