Cardiac dysrhythmia is a term for any of large heterogeneous group of conditions in which there is abnormal electrical activity in the heart. Dysrhythmias may be life threatening medical emergencies that can result in cardiac arrest and sudden death; it may predispose the patient to potentially life threatening stroke and embolism. The pathogenesis of cardiac dysrhythmia involves crossing of electrolytes through different ions channels on the cellular level that may be dysrhythmogenic. In this study, ischemic-reperfusion dysrhythmia were performed in experimental animals, ischemia of the myocardium results in release of ischemic metabolites and slowing impulse propagation while reperfusion results in increase late inward Na current (INaL) which amplifies Na + influx and intracellular Na + concentration leading finally to calcium overload. The enhancement of Na + and Ca2 + concentration causes electrophysiological instability, formation of free oxygen radicle and liberation of platelet activating factor. Seeking for novel antidysrhythmogenic agents having ions channels inhibiting properties, this work aims to investigate the effects of vernakalant, antidysrhythmic drug with atrial selective and multichannel blocking effect on ischemia-reperfusion dysrhythmia in experimental animals in comparison with amiodarone as a standard antidysrhythmic medication.
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