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Objectives Investigated the cardioprotective and mechanisms of losartan onwhole isolated ischemic reperfused rat heart. Meth-ods Langendorff perfused systems was used to in-vestigate losartan effect on whole isolated rat hearts inCPK, LDH, MDA, SOD, ang Ⅱ and arrhythmia. Re-sults Losartan decreased incidence of arrhythmia,improved atrial ventricular block recovery in reperfu-sion period, during ischemic period, CPK and LDH inI/R group increased significantly compared with con-trol group, 51.33±27.02 vs 22.42±13.33, 31.80±4.56 vs 22.28 ± 15.96, respectively, but greatlydecreased in losartan group compared with I/R group,23.90±21.74 vs 51.33±27.02 and 11.50±13.20vs 31.80 ± 4. 56, respectively. During reperfusion pe-riod CPK, LDH increased significantly in I/R groupcompared with control group, 49.11 ± 20.63 vs 12.14±5.92 and 28.70±4.69 vs 23.10±21.38, re-spectively, but decreased greatly in losartan groupcompared with I/R group, 39.40 ± 9.60 vs 49.11 ±20.63 and 14.50±13.75 vs 28.70±4.69. Thecontent of MDA, ang Ⅱ in I/R group myocytes ishigher than control group’s , 26. ±9. 25 vs 17.2 ±3.37 and 8.43±3.81 vs 4. 80±0.20. However thecontent of SOD in two groups has no significantlychange, 148. 20 ± 8. 72 vs 145.08±6.82. the con-tent of MDA in losartan group myocardial tissue ismuch lower than control group, 15.92±4.05 vs26.80± 9.25 and the content of ang Ⅱ in losartangroup myocardial tissue is much higher than I/Rgroup, 12.44 ± 6.09 vs 8.43 ± 3.21. The departmentof cardiology of second hospital of Tianjin medical u-niversity Tianjin 300211 However, SOD has nosignificant change in two groups, 143.47 ±7.91 vs145.08 ± 6.82. Conclusions Losartan against is-chemic-reperfusion injury of whole isolated rathearts, those beneficial effects are mediate primarily bythe inhibited of angiotensin Ⅱ binding with its receptorand inhibited oxygen free radical scavenging potential.