Summary: In order to study the effects of losartan on cardiomyocyte apoptosis following ischemia (0. 5 h) and reperfusion (48 h) in vivo and bcl-2 and bax gene expression, TUNEL staining method, immunohistochemistry and in situ hybridization histochemistry (ISHH) were used to monitor the apoptotic cells, mRNA and protein of gene expression, respectively. Image processing system was used to quantitively dispose the positive metric substance of both immunohistochemistry and ISHH through the average optical density (OD) value. The number of the apop- totic cells were 38±9 (control group), 0-1 (sham operation group) and 9±4 (losartan-treated group) in each visual field respectively with the difference among the groups being significant (P< 0. 001 ). OD values of bcl-2 (ISHH) were 0. 07425± 0. 02029 (control group ), 0. 05961± 0. 009932 (sham operation group) and 0. 07619±0. 01445 (losartan-treated group ) respectively, while OD values of bcl-2 (immunohistochemistry) were 0. 1374±0. 01367 (control group ), 0. 08510±0. 01862 (sham operation group) and 0. 1252±0. 02064 (losartan-treated group). hcl-2 gene expression was increased significantly in the control group and losartan-treated group as com- pared with sham operation group (P < 0. 05 ). OD value of bax (immunohistochemistry) was 09727±0. 02230 (control group), 0. 06182±0. 01430 (sham operation group) and 0. 06213± 0. 01420 (losartan-treated group). bax gene expression was decreased very significantly in losartan-treated group and sham operation group as compared with control group (P<0. 001 ). Bcl-2/ bax ratio was 1. 413 (control group), 1. 376 (sham operation group) and 2. 016 (losartan-treated group) respectively. The results indicated that losartan might inhibit cardiomyocyte apoptosis following ischemia and reperfusion. The mechanism might be that bax gene expression was inhibited to increase bcl-2/bax ratio. Summary: In order to study the effects of losartan on cardiomyocyte apoptosis following ischemia (0.5 h) and reperfusion (48 h) in vivo and bcl-2 and bax gene expression, TUNEL staining method, immunohistochemistry and in situ hybridization histochemistry ) were used to monitor the apoptotic cells, mRNA and protein of gene expression, respectively. respectively. Image processing system was used to quantitively dispose the positive metric substance of both immunohistochemistry and ISHH through the average optical density (OD) value. The number of the apop - totic cells were 38 ± 9 (control group), 0-1 (sham operation group) and 9 ± 4 (losartan-treated group) in each visual difference respectively the groups are significant (P <0.001) Respectively. 0 OD values ​​of bcl-2 (ISHH) were 0. 07425 ± 0. 02029 (control group), 0. 05961 ± 0. 009932 (sham operation group) and 0. 07619 ± 0. 01445 (losartan-treated group) , while OD values ​​of bcl-2 (immunohistochemistry) were 0. 1374 ± 0. 01367 (control group), 0. 08510 ± 0. 01862 (sham operation group) and 0. 1252 ± 0. 02064 (losartan-treated group). Hcl-2 gene expression was significantly increased in the control group and losartan-treated group The value of bax (immunohistochemistry) was 09727 ± 0. 02230 (control group), 0. 06182 ± 0. 01430 (sham operation group) and 0. 06213 ± 0. 01420 (losartan-treated group). Bax gene expression was decreased very significantly in losartan-treated group and sham operation group as compared with control group (P <0.001). Bcl-2 / bax ratio was 1. 413 The results suggest that losartan might inhibit cardiomyocyte apoptosis following ischemia and reperfusion. The mechanism might be that bax gene expression was inhibited to the control group, 1. 376 (sham operation group) and 2. 016 (losartan-treated group) respectively. increase bcl-2 / bax ratio.