Objective        To study the correlation between protective effect of low pH solution reperfusion on myocardial ischemia/reperfusion (I/R) and expression of Bcl-2 and Bax in rabbits undergoing extracorpor

eal circulation.       Methods        Thirty adult New Zealand white rabbits were randomly divided into control group

I/R group

pH 7.4 group

pH 6.9 group

and post-ischemia conditioning group (6 in each group). Rabbits in control group underwent extracorporeal circulation for 180 min

those in I/R group underwent reperfusion for 120 min after 40 min of myocardial ischemia

those in pH 7.4 group and pH 6.9 group received a K-H solution at 37 ℃ containing 95%O

2

+5%CO

2

at pH 7.4 or pH 6.9 in 2 min before they underwent reperfusion

and those in post-ischemia conditioning group were conditioned 2 min before they underwent reperfusion. Changes in their myocardial morphology were observed under light microscope

their serum cardiac troponin I (cTnI) level was measured by ELISA

expressions of Bcl-2 and Bax mRNA and protein were detected by RT-PCR and immunohistochemistry

respectively.       Results        The myocardial tissue injury was milder and the cTnI level was lower in pH6.9 group and post-ischemia conditioning group than in I/R group (0.648 2±0.070 8 vs 1.058 1±0.165 7

0.156 5±0.019 2 vs 0.233 1±0.022 5

P0.05）. The expression level of Bcl-2 mRNA and protein was significantly higher and the expression level of Bax mRNA and protein was significantly lower in pH 6.9 group than in I/R group and post-ischemia conditioning group（1.058 1±0.165 7 vs 0.648 2±0.070 8 and 0.233 1±0.022 5 vs 0.156 5±0.019 2

1.353 3±0.138 1 vs 1.901 7±0.198 1 and 0.173 5±0.015 1 vs 0.247 1±0.021 3

P0.05）. No significant difference was found in expression level of Bcl-2 and Bax mRNA and protein between pH6.9 group and post-ischemia conditioning group (P0.05).       Conclusion        Transient low pH solution reperfusion can protect heart against I/R injury in rabbits undergoing extracorporeal circulation by mimicking the post-ischemic conditioning and regulating the expression of Bcl-2 and Bax.