Summary: Whether conventional hypothermic CPB induces myocyte apoptosis in dog hearts and modulation of bcl-2, bcl-xl, bax, bad, and caspase-3 pathways in this setting was investigated. Ten healthy adult dogs were randomized into sham-operated and CPB groups. Samples of left ventricle were obtained before, during and 3 h after CPB. In situ TUNEL was used to detect apoptotic my ocytes. Immunohistochemistry and flow cytometry were employed for detection of expressions of bcl 2, bcl-xl, bax and bad proteins. Z-DEVD-AMC substrate cleavage and TBARS methods were usedto measure the activity of caspase-3 and the content of lipid peroxide in LV myocardium, respective ly. After CPB, the number of apoptotic myocytes in CPB group was significantly increased. The re-sults of immunohistichemistry demonstrated that bcl-2, bcl-xl, bax and bad proteins were constitu tionally presnt on the sarcolemma of the LV myocytes. FACS results showed that, after CPB, ex-pressions of bax and bad in CPB group were significantly upregulated, while the expressions of bcl-2 and bcl-xl were not significantly changed in both groups. The activity of caspase-3 and the content of lipid peroxide in LV myocardium in CPB group were also significantly increased after CPB. The pre-sent study shows that there exists myocardiocyte apoptosis in dog hearts undergoing conventional hy-pothermic CPB and the myocyte apoptosis is initiated by ischemia and performed during reperfusion.Moreover, the CPB-induced myocyte apoptosis was associated with upregulation of expressions of bax and bad proteins, activation of caspase-3 and increase of oxidative stress.