The Impact Of Sufentanil To The Toll-like Receptor4(TLR4)and Tumor Necrosis Factor-alpha (TNF-α) In Myocardial Ischemia-reperfusion

Object:To observe the impact of sufentanil on the Toll-like receptor4(TLR4) and tumor necrosis factor-alpha (TNF-α) in myocardial ischemia-reperfusion.Discuss the protection mechanism of sufentanil on myocardial ischemia and reperfusion injury protection mechanismMethods:40Wistar rats were randomly divided into sham operation group, ischemia-reperfusion group,ischemic-treatment group and drug-treatment group.Prepared the model of myocardial ischemia-reperfusion injury by ligaturing the rat coronary heart left anterior descending (LAD). Sham operation group:the LAD were stringed without ligating; Ischemia-reperfusion group:the LAD subjected to30min of myocardial ischemia followed by120min of reperfusion; Ischemic-treatment group:5min before refusion, the LAD were given ischemia3’-reperfusion3’three times; Drug-treatment group:5min before refusion, the LAD were given sufentanil0.1ug/kg.Immunohistochemical assay the contents of the Toll-like receptor4in the myocardium of rat and the tumor necrosis factor-a in the determined serum.Results:The content of Toll-like receptor4and tumor necrosis factor-α content of the sham operation group was lower than that of the other three groups,the differences were statistically significant (P<0.05).that of Drug-treatment group lower than the ischemic-treatment group and ischemia-reperfusion group, the differences were statistically significant (P<0.05). Ischemic-treatment group was lower than ischemia-reperfusion group, the differences were statistically significant (P<0.05).Ischemia-reperfusion group was higher than that of the other three groups,the differences were statistically significant (P<0.05).Conclusions:There was a protection mechanism of sufentanil on myocardial ischemia-reperfusion injury.TLR4was involved in the formation of myocardial ischemia-reperfusion injury.Sufentanil may have an important influence on TNF-α And may inhibit the expression of TLR4signal transduction.