The effect of propofol preconditioning on cytochrome C release from mitochondria during hypoxia/reoxygenation in isolated rat hearts

Aim To explore the effect of propofol preconditioning on cardiocyte apoptosis and cytochrome C release from mitochondria during hypoxia/reoxygenation in isolated rat hearts.Methods Fifty male Sprague-Dawley rats weighing 250～300 g were randomly divided into 5 groups(n=10 each):control group(C);Dimethyl sulfoxide(DMSO)preconditioning group(D);3 propofol preconditioning groups with 25 μmol·L-1(P1)、50 μmol·L-1(P2)、100 μmol·L-1(P3)propofol respectively.The isolated rat hearts were retrogradely perfused via aorta with K-H solution on Langendorff apparatus.The isolated hearts were made hypoxia for 30 minutes followed by 60 minutes reoxygenation in each group.The D,P1,P2,P3 groups were preconditioned by perfusing 10 min K-H solution containing 20 μmol·L-1 DMSO and 25,50,100 μmol·L-1 propofol respectively and then followed by 5 min K-H solution reperfusion before hypoxia.The preconditioning procedure was repeated twice.The cardiac functional variables were recorded after equilibration(baseline values),immediately before hypoxia,at the end of 30 min and 60 min reoxygenation.Apoptotic myocardial cells were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling(TUNEL)and the level of cytochrome C expression in myocardial cytosol and mitochondria was measured by Western blot at the end of reoxygenation.Results At the end of 30 min and 60 min reoxygenation,LVEDP was significantly lower and LVDP was significantly higher in P1,P2,P3 groups than in D group(P0.05).Apoptosis rate decreased significantly in P1,P2,P3 groups than in D group at the end of reoxygenation(P0.05 or 0.01).Cytochrome C level increased significantly in mitochondria but decreased significantly in cytosol in P1,P2,P3 groups as compared with D group(P0.05 or 0.01).There was no significant difference between D group and C group.Conclusions Propofol preconditioning can decrease cardiocyte apoptosis and protect the heart against hypoxia/reoxygenation injury by its attenuation of the release of cytochrome C from mitochondria to cytosol.