The purpose of this study was to determine the utility of the monophasic action potential (MAP) changes as an arrhythmic biomarker in hypothermic ischemia-reperfusion. The hypothermic ischemia-reperfusion model was subjected to 60 min of cardioplegic arrest while the isolated rat hearts were preserved with a multidose cold K-H solution at 4 °C. During the reperfusion period, the heart's arrhythmia and monophasic action potential were also monitored. The myocardial damage was assessed using HE and TTC stains. Immunohistochemistry and Western blotting were used to assess the expression and distribution of Connexin 43 (Cx43) and Akt. Collectively, prolonged action potential durations, increased dispersion of repolarization, and downregulated and lateralized Cx43 all contribute to the derangement of electrical impulse propagation that may underlie arrhythmogenesis in the cold ischemic heart following cardioplegic arrest. MAP might be used as a biomarker for arrhythmias caused by hypothermic ischemia-reperfusion.
Keywords: Cardiac arrest; Cardioplegia; Connexin 43; Hypothermic reperfusion arrhythmias; Monophasic action potential.
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