Objective To investigate the effects of lidocaine on sevoflurane postconditioning-induced cardioprotection and detect its potential mechanism.　Methods　Chose healthy adult male Sprague-Dawley rats. Their hearts were excised and perfused in a Langendorff apparatus. After 20 min of equilibration, the hearts subjected to 40 min of ischemia followed by 120 min of reperfusion, then randomly divided into the following seven groups （n=6 each）： Sham-operation （Sham）， ischemia/reperfusion （I/R）， ischemia/reperfusion and 20 mg/L lidocaine（I/R+Lid-20）， sevoflurane postconditioning（SPC）， SPC and 2， 10 or 20 mg/L lidocaine（SPC+Lid-2， SPC+Lid-10， SPC+Lid-20）. After 20 min of equilibration， the hearts subjected to 40 min of ischemia followed by 120 min of reperfusion. left ventricular developing pressure（LVDP）， left ventricular end-diastolic pressure（LVEDP）， heart rate （HR）， maximal rise/fall rate of left ventricular pressure （±dp/dtmax） and coronary artery flow（CF） were recorded continuously. Coronary effluent was collected at 5 and 10 min of reperfusion for determination of lactate dehydrogenase（LDH） and creatine kinase（CK） activities. Myocardial tissues were obtained at the end of reperfusion for determination of infarct size（IS） and related proteins. 　Results　The LVDP， dp/dtmax ， CF were significantly higher and LVEDP， LDH and CK activities， IS ［（23.9±1.4）%， （20.5±1.3）%， （24.7±2.1）% vs （47.9±3.3）%］ were markedly lower in the SPC， SPC+Lid-2， SPC+Lid-10 groups than in the I/R group at all points of reperfusion （P<0.05）; Compared with group I/R， all the measures were not significantly different in the I/R+Lid-20 and SPC+Lid-20 groups （P>0.05）;The SPC group increased the expression of p-Akt， p-Erk1/2 and Bcl-2， but 20 mg/L lidocaine abolished the increased expression of Bcl-2 induced by SPC. 　Conclusions　20 mg/L lidocaine inhibits the protective effect induced by SPC and inhibition of Bcl-2 expression may be involved in.