Effects of sevoflurane postconditioning on expression of cardiomyocyte p70S6K during ischemia-reperfusion in isolated rat hearts / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effects of sevoflurane postconditioning on the expression of 70 kD aribosomalprotein S6 kinase (p70S6K) during ischemia-reperfusion (I/R) in isolated rat hearts.Methods Pathogen-free male Sprague-Dawley rats,aged 3 months,weighing 270-350 g,were used in the study.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95 ％ O2-5 ％ CO2.Ninety isolated rat hearts with I/R injury were randomly divided into 3 groups (n =30 each)sham operation group (group S),I/R group (group I/R),and sevoflurane postconditioning group (group SP).The hearts were subjected to ischemia for 30 min followed by 2 h reperfusion.In group SP,the hearts were perfused with K-H solution saturated with 3.0％ sevoflurane for 15 min starting from the end of ischemia until 15 min of reperfusion,and then with plain K-H solution for 105 min.At 2 h of reperfusion,myocardial infarct size was measured,the percentage of myocardial infarct size was calculated,and the phosphorylated p70S6K (p-p70S6K)/total p70S6K (tp70S6K) ratio,and cytoplasm,cytochrome C,and caspase-8 expression was measured.Results Compared with group S,the percentage of myocardial infarct size and p-p70S6K/t-p70S6K ratio were significantly increased,the expression of cytochrome C,and caspase-8 was up-regulated,and the expression of cytochrome C was downregulated in I/R group.Compared with I/R group,the percentage of myocardial infarct size was significantly decreased,the ratio of p-p70S6K/t-p70S6K was increased and cytochrome C expression was up-regulated,and the expression of cytochrome C and caspase-8 was down-regulated in SP group.Conclusion Sevoflurane postconditioning can mitigate I/R injury to isolated rat hearts,and up-regulation of p-p70S6K expression,inhibition of transfer of cytochrome C from mitochondria to cytoplasm,and reduced cell apoptosis are involved in the mechanism.