The primary electrophysiological effects of mori-cizine relate to its inhibition of the fast inward sodium channel. Moricizine reduces the maximal upstroke of phase 0 and shortens the cardiac transmembrane action potential. The sodium channel blocking effect of mori-cizine is more significant at faster stimulation rates; an action referred to as use dependence. This phenomenon may explain the efficacy of moricizine in suppressing rapid ectopic activity. An interesting effect of moricizine is its depressant effect on automaticity in ischemic
Purkinje tissue in contrast to its inability to alter the slope of phase 4 depolarization of spontaneous automatic Purkinje fibers.
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