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The present study was designed to investigate the negative inotropic effects of gaseous SO<jats:sub>2<\/jats:sub> and its derivatives in the isolated perfused rat heart and the possible mechanisms involved in their effects. The results showed that both SO<jats:sub>2<\/jats:sub> and SO<jats:sub>2<\/jats:sub> derivatives elicited a negative inotropic effect in a dose\u2010dependent manner, and SO<jats:sub>2<\/jats:sub> produced a higher negative effect than SO<jats:sub>2<\/jats:sub> derivatives. The mechanism of SO<jats:sub>2<\/jats:sub>\u2010induced negative inotropic effects at low concentrations was different from that at high concentrations. At low concentrations, the mechanism of SO<jats:sub>2<\/jats:sub>\u2010induced negative inotropic effects might occur through promoting the activities of protein kinase C (PKC), cycloxygenase, and cGMP, while the mechanism of SO<jats:sub>2<\/jats:sub> derivatives\u2010induced effects might be related to the opening of ATP\u2010sensitive K<jats:sup>+<\/jats:sup> (K<jats:sub>ATP<\/jats:sub>) channel and the inhibition of Ca<jats:sup>2+<\/jats:sup> influx via L\u2010type calcium\u2010channel. At high concentrations, the mechanisms of SO<jats:sub>2<\/jats:sub> and SO<jats:sub>2<\/jats:sub> derivatives\u2010induced negative inotropic effects were similar, which might be related to the K<jats:sub>ATP<\/jats:sub> channel and L\u2010type calcium\u2010channel as well as the possible alterations in PKC, cycloxygenase, and cGMP. Further work is needed to determine the relative contribution of each pathway in SO<jats:sub>2<\/jats:sub>\u2010mediated inotropic effect. \u00a9 2010 Wiley Periodicals, Inc. 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