Objective: To elucidate the possible mechanism responsible for the improved protection of terminal warm blood cardioplegia (TWBC) after hypothermic cardiopulmonary bypass (CPB) through analysis of tubulin (TB) components changes in myocardial cells exposed to TWBC. Methods: Stable animal models of CPB were established in cats, which were then randomly divided into 2 groups. Group Ⅰ was subjected to intermittent cold blood cardioplegia (ICBC) whereas group Ⅱ to ICBC followed by TWBC before uncross-clamping. Left ventricular performance was then monitored and evaluated by LVSP, LVEDP, ±dp/dtmax and t-dp/dtmax in both groups and semi-quantitive analysis was conducted with Western blot method as to the content and constitution of TB in myocardial cells at 15 min, 120 min after aortic crossclamping (ACC) and 5 min,15 min, 60 min,120 min after reperfusion. Results: Within 120 min after reperfusion, systolic and diastolic functions decreased significantly in group Ⅰ as compared with group Ⅱ(P<0.05). At 115 min after ACC and 15 min after reperfusion, the content of free and polymerized TB in both groups had no difference (P>0.05). At 120 min after ACC and 5 minutes after reperfusion, there was a significant difference between groupⅠ andⅡ (P<0.01). Conclusion: TWBC accelerates the repolymerization of myocardial TB during hypothermic CPB, which may mediate the improved cardiac performance in the early stage of myocardial reperfusion.