The negative inotropic effects of gaseous sulfur dioxide and its derivatives in the isolated perfused rat heart.

Epidemiological investigations have revealed that sulfur dioxide (SO(2) ) exposure is linked to cardiovascular diseases. The present study was designed to investigate the negative inotropic effects of gaseous SO(2) and its derivatives in the isolated perfused rat heart and the possible mechanisms involved in their effects. The results showed that both SO(2) and SO(2) derivatives elicited a negative inotropic effect in a dose-dependent manner, and SO(2) produced a higher negative effect than SO(2) derivatives. The mechanism of SO(2) -induced negative inotropic effects at low concentrations was different from that at high concentrations. At low concentrations, the mechanism of SO(2) -induced negative inotropic effects might occur through promoting the activities of protein kinase C (PKC), cycloxygenase, and cGMP, while the mechanism of SO(2) derivatives-induced effects might be related to the opening of ATP-sensitive K(+) (K(ATP) ) channel and the inhibition of Ca(2+) influx via L-type calcium-channel. At high concentrations, the mechanisms of SO(2) and SO(2) derivatives-induced negative inotropic effects were similar, which might be related to the K(ATP) channel and L-type calcium-channel 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(2) -mediated inotropic effect.