Objective      To investigate the protective effect of propofol postconditioning on myocardium against ischemia-reperfusion injury in isolated rat hearts and the role of PI3K/Akt signaling pathway.       Methods       Twenty-eight rats were randomly divided into four groups including an ischemia-reperfusion group (I/R group)

a

propofol postconditioning group (PPC group)

a propofol postconditioning combined with wortmannin group (PPC+W group) and a wortmannin group (W group). The I/R models of isolated hearts were established in all of the groups. The LVEDP and  dp/dt

max

were measured before ischemia and at 120 min after reperfusion. The expression of Bcl-2 was measured by immunohistochemistry

the apoptotic index was measured by TUNEL

and the expression of p-Akt (Ser473) was measured by Western blotting.       Results        Compared with the I/R group

the LVEDP significantly decreased (43.31±4.70 vs 29.93±3.72

P0.05)

and +dp/dt

max

and -dp/dt

max

significantly increased in the PPC group (1 140±138 vs 1 622±160; 749±99 vs 1 008±178

P0.05). The expression of Bcl-2 and p-Akt in the myocardium of the PPC group was significantly higher than that of the I/R group (0.171 9±0.012 1 vs 0.199 1±0.014 4; 0.241 4±0.053 9 vs 0.436 3±0.081 7

P0.05)

while the proportion of apoptotic cardiomyocytes decreased significantly in the PPC group as compared with the I/R group (33.87±1.72 vs 29.84±1.83

P0.05). Wortmannin could block the protective effect of propofol postconditioning (P0.05).       Conclusion        Propofol postconditioning could attenuate the apoptosis in the isolated heart induced by I/R probably through PI3K/Akt signal pathway and Bcl-2 upregulation.