Effect of cimetidine on isolated rat myocardial reperfusion injury

The effects of cimetidine (Cim) on ventricular fibrillation threshold (VFT),diastolic excitation threshold (DET), effective refractory period (ERP), andvulnerable period (VP), were determined in both stable perfusion and postischemic reperfusion rat hearts. The results showed that reperfusion after 15 min global myocardial ischemia caused a significant decrease VFT and ERP, and an increase in VP and DET. Cim 1 mmol.L-1 prevented the lowering in VFT, shortening in ERP, and lengthening in VP from the postischemic reperfusion. Cim 0.1 mmol.L-1 attenuated the exacerbation of VFT and VP. Cim 0.01 mmol.L-1 did not exert any noticeableinfluence on the electrophysiological parameters. It was shown that Cim 1mmol.L-1 protected myocardium against the aggravation of electrophysiologicalcharacteristics induced by postischemic reperfusion.