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Exogenous SO 2 is toxic especially to the pulmonary and cardiovascular system, similar to nitric-oxide, carbon-monoxide, and hydrogen-sulfi de. Endogenous SO 2 is produced in many cell types. The SO 2 content of the rat heart has been observed to substantially decrease during isoproterenol-induced hypertrophy. This study sought to determine whether an SO 2 derivative could inhibit the prolongation of action potentials during the isoproterenol-induced hypertrophy of rat cardiomyocytes and explore the ionic currents. Alongside electrocardiogram recordings, the voltage and currentclamped measurements were conducted in the enzymatically isolated left ventricular cardiomyocytes of Wistar rats. The consistency of the results was evaluated by the novel mathematical electrophysiology model. Our results show that SO 2 signifi cantly blocked the prolongation of QT-interval and action potential duration. Furthermore, SO 2 did not substantially affect the Na + currents and did not improve the decreased steadystate and transient outward K + currents, but it reverted the reduced L-type Ca 2+ currents (I CaL ) to the physiological levels. Altered inactivation of I CaL was remarkably recovered by SO 2 . Interestingly, SO 2 signifi cantly increased the Ca 2+ transients in hypertrophic rat hearts. Our mathematical model also confi rmed the mechanism of the SO 2 effect. Our fi ndings suggest that the shortening mechanism of SO 2 is related to the Ca 2+ dependent inactivation kinetics of the Ca 2+ current.

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