摘要
Objective:To explore the protective effect of remifentanil on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury and their possible mechanism. Methods:The model of rat hepatic ischemia-reperfusion injury was used and the effect of remifentanil on the ultrastructure of mitochondria, calcium homeostasis, MDA level in mitochondria were observed. Results: In contrast with the control group, mitochondrial matrix calcium concentration, calcium concentration after calcium uptake, and the quantity of calcium uptake in low and high remifentanil concentration groups and 5-HD group are lower (P<0. 01), and there is no difference in RHD (5-HD+remifentanil) group. The difference in MDA level between groups is insignificant. Conclusion:Remifentanil at clinical concentrations exerts a protective effect on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury, in which activating the KATP channel may be involved.
Objective：To explore the protective effect of remifentanil on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury and their possible mechanism. Methods：The model of rat hepatic ischemia-reperfusion injury was used and the effect of remifentanil on the ultrastructure of mitochondria, calcium homeostasis, MDA level in mitochondria were observed. Results： In contrast with the control group, mitochondrial matrix calcium concentration, calcium concentration after calcium uptake, and the quantity of calcium uptake in low and high remifentanil concentration groups and 5-HD group are lower （P〈0.01）, and there is no difference in RHD （5-HD＋remifentanil） group. The difference in MDA level between groups is insignificant. Conclusion ：Remifentanil at clinical concentrations exerts a protective effect on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury, in which activating the KATP channel may be involved.
