The effect of propofol preconditioning on cytochrome C release from mitochondria after mild hypothermic ischemia/reperfusion in isolated rat hearts / 中国应用生理学杂志

ABSTRACT

<p><b>AIM</b>To explore the effect of propofol preconditioning on cardiomyocyte apoptosis and cytochrome C release from mitochondria during mild hypothermic ischemia/reperfusion in isolated rat hearts.</p><p><b>METHODS</b>50 isolated SD rat hearts perfused on Langendorff apparatus were randomly divided into 5 groups (n=10) control group (C), DMSO group (D), 3 different concentrations of propofol groups of 25 micromol x L(-1) (P1), 50 micromol x L(-1) (P2), 100 micromol x L(-1) (P3) propofol respectively. All of the isolated rat hearts were subjected to 31 degrees C mild hypothermic ischemia for 55 min followed by 60 min reperfusion. The D, P1, P2, P3 groups were preconditioned by perfusing with K-H solution containing 20 micromol x L(-1) DMSO and 25, 50, 100 micromol x L(-1) propofol respectively for 10 min and then followed by 5 min K-H solution washing out before ischemia. The preconditioning procedure was repeated twice. Hemodynamics of the hearts was recorded after equilibration(baseline values) immediately before ischemia, 30 min and 60 min after reperfusion respectively. Cardiomyocyte apoptosis rate and contents of cytosolic and mitochondrial cytochrome C were measured at the end of reperfusion.</p><p><b>RESULTS</b>After 30 min and 60 min reperfusion, LVEDP was significantly lower and LVDP was significantly higher in P3 group than those in C group ( P < 0.05, P < 0.01). Compared with C group, cardiomyocyte apoptosis rate of the hearts decreased significantly in P2,P3 groups at the end of reperfusion (P < 0.05, P < 0.01). Cytochrome C level increased significantly in mitochondria but decreased significantly in cytosol in P2, P3 groups as compared with C group (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>Propofol preconditioning decreased cardiomyocyte apoptosis, protected the heart against 31 degrees C mild hypothermic ischemia/reperfusion injury by attenuation of the release of cytochrome C from mitochondria to cytosol.</p>