[Effect of sufentanil preconditioning on myocardial P-Akt expression in rats during myocardial ischemia-reperfusion].

OBJECTIVE: To study the protective effect of sufentanil preconditioning against myocardial ischemia-reperfusion (I/R) injury and the role of PI3K/Akt signaling pathway. METHODS: Sixty male SD rats weighing 250-350 g were randomly divided into 5 equal groups, namely the sham-operated group, I/R group, sufentanil preconditioning group (Spc group), sufentanil preconditioning +PI3K inhibitor group (Spc+W group), and PI3K inhibitor group (W group). Myocardial I/R model was established by ligation of the anterior descending branch of the left coronary artery for 30 min followed by reperfusion for 120 min. Sufentanil was administered in 3 doses via the femoral vein before the occlusion, each at 1 µg/kg infused within 5 min at a 5-min interval. In Spc+W and W groups, PI3K inhibitor wortmannin (15 µg/kg) was given intravenously 5 min before sufentanil preconditioning and 35 min before ischemia, respectively. Heart rate and mean arterial pressure (MAP) were continuously monitored during I/R. At the end of reperfusion, blood samples were obtained to determine plasma activation of CK-MB and LDH. Acute infarct size was measured by triphenyltetrazolium chloride staining, and the myocardial tissues were obtained to detect the expression of phosphorylated Akt using Western blotting. RESULTS: Phosphorylated Akt expression was significantly up-regulated in I/R and Spc groups as compared with the sham group, and was significantly higher in Spc group than in I/R group. After reperfusion, sufentanil preconditioning significantly decreased myocardial infarct size (P<0.01) and lowered the levels of CK-MB (P<0.01) and LDH (P<0.01) compared with those in the I/R group. The I/R , Spc+W and W groups showed no significant differences in myocardial infarct size or the levels of CK-MB and LDH. CONCLUSION: The protective effect of sufentanil preconditioning against myocardium against I/R injury in rats may involve PI3K/Akt signaling pathway activation.