Recainam

Recainam (Wy-42362) is a potent orally active antiarrhythmic agent and a sodium channel inhibitor. Recainam elevates ventricular fibrillation threshold, suppresses induced cardiac dysrhythmias, and may accentuate cardiac tissue refractoriness heterogeneity. Recainam can be used for the research of arrhythmias^[1][2][3][4]. In Vitro:Recainam (10-300 μM; ≥30 min) has no significant effect on key electrophysiologic variables of isolated rabbit sinoatrial node preparations, aside from modestly shortening action potential duration^[2].
Recainam (10-100 μM; ≥30 min) significantly reduces the maximal rate of rise of phase 0 (V̇max) in isolated rabbit atrial muscle preparations without altering other key electrophysiologic variables^[2].
Recainam (10-300 μM; ≥30 min) causes concentration-dependent reductions in the maximal rate of rise of phase 0 (V̇max) in isolated canine ventricular muscle preparations without altering action potential duration or effective refractory period^[2].
Recainam (1-300 μM; ≥30 min) causes concentration-dependent reductions in the maximal rate of rise of phase 0 (V̇max), action potential amplitude, action potential duration, and effective refractory period in isolated canine Purkinje fiber preparations^[2].
Recainam (10-60 μM; ≥30 min) shifts the membrane responsiveness curve in the hyperpolarizing direction in isolated canine Purkinje fiber preparations, with higher concentrations abolishing premature responses from depolarized membrane potentials^[2].
Recainam (300 μM; ≥30 min) induces a frequency-dependent reduction in the maximal rate of rise of phase 0 (V̇max) in isolated canine Purkinje fiber, canine ventricular muscle, and rabbit atrial muscle preparations, and abolishes responses at frequencies >3 Hz in Purkinje fibers^[2].
Recainam (100 μM; ≥10 min) depresses phase 4 depolarization and slows isoproterenol-induced automaticity in isolated canine Purkinje fiber preparations^[2].
Recainam (300 μM; ≥30 min) does not affect slow channel-dependent potentials induced by high potassium and isoproterenol in isolated canine ventricular muscle and Purkinje fiber preparations^[2]. In Vivo:Recainam (3.75-7.5 mg/kg loading; 0.0375-0.075 mg/kg per min maintenance; i.v.; loading dose over 20 min; maintenance infusion for remainder of experiment) elevates the energy required for ventricular defibrillation in a dose-dependent manner, with low and high doses increasing E₅₀ by 42% and 92%, respectively, while prolonging QRS duration without altering ventricular effective refractory period^[1].
Recainam (p.o.; i.v.) exhibits anti-arrhythmic activity in dogs with experimentally induced cardiac arrhythmias^[3].