the data confirmed that continuous perfusion with NaHS at a dosage of 100 mmol/L following nifedipine perfusion might increase the ventricular 6dp/dtmax and DLVP. The LV 6dp/dtmax and DLVP decreased after perfusion with DM at dose of 100 mmol/L for 5 min as compared with controls. Nevertheless, while in the presence of DM perfusion fluid, the LV 6dp/dtmax and DLVP weren’t improved when constantly perfused with 100 mmol/L NaHS for 10 min. Next, we used DTT, a lowering sulfhydryl modifier, in the perfusion fluid to see if it may mediate the inhibition Hedgehog inhibitor of cardiac function induced by NaHS. Additionally to the actual fact that LV 6dp/ dtmax and DLVP did not change during perfusion with 100 mmol/ L DTT for 5 min as compared with controls, we found that continuous perfusion of K H solution with 100 mmol/L NaHS for 10 min in the presence of DTT certainly lowered the LV 6dp/dtmax and DLVP, compared to DTT perfusion without NaHS treatment. The result of nifedipine on cardiac function in isolated perfused rat hearts addressed by NaHS Compared with controls, the LV 6dp/dtmax and DLVP diminished when perfused with the K H solution consisting of nifedipine in a dosage of 10 mmol/L for 5 min. Nevertheless, after steady perfusion Extispicy with the K H solution for 10 min, the ventricular 6dp/dtmax and DLVP improved notably as compared to those with K H solution composed of nifedipine. However, there were no significant differences in the change in the ventricular 6dp/ dtmax and DLVP between the perfusate with and without NaHS following nifedipine perfusion. Those results suggested that pretreatment with nifedipine to prevent LCa 2-channel can prevent the negative inotropic effect of NaHS. Characteristics ATP-competitive Chk inhibitor of the L type calcium channel current in rat ventricular cardiomyocytes. This inward current could be almost totally inhibited by 10 mmol/L nifedipine, a particular L type calcium-channel blocker, and could be improved significantly by 1 mmol/L Bay K 8644. The top of the I V curve of the I Ca, M was at membrane potentials of 0 mV in order conditions and bath application of 1 mmol/L Bay K 8644. Inhibitory influence of NaHS on I Ca, L in rat ventricular cardiomyocytes I Ca, L was elicited by pulses from a holding potential of 240 mV to 0 mV for 200 ms every 1 minute utilizing the whole cell patch clamp technique. Four increasing concentrations of NaHS were successively used to the cell for 3 min duration of perfusion per awareness, and the effects of NaHS about the I Ca, L were detected. The inhibition of I Ca, L beat quickly within the first 1 minute, and through the time I Ca, L may be partially recovered. Thus, the consequences of NaHS on I Ca, L were reversible at the very least partly. Attention dependent inhibitory influence of NaHS on I Ca, L As shown in Fig.