ABSTRACT
Objective To explore the mechanism of the catdioprotection of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury in rabbits.Method Thirty male New Zealand white rabbits,weighing 2.0 to 2.5 kg,were randomly divided into three groups(ten for each group):Control group(group C),I/R group(I/R group) ,2.0% isoflurane group(group S) .Group S was exposed to 2.0% isoflurane-100% oxygen for2 h.Group C and I/R group were exposed 2 h to 100% oxygen served as untreated controls.Twenty-four hours later I/R group and group S underwent 40 rain of coronary occlusion followed by 2 h of reperfusion.Blood samples were taken from arterial line at 20 min before occlusion(T1) ,20 rain after occlusion(T2) ,40 rain after occlusion(T3) ,1 h after reperfusion(T4) and 2 h after reperfusion(TS) for determination of plasma IL-10 levels and TNF-alevels by ELISA.At the end of the reperfusion,infarct size and area at risk were defined by Evans and TTC staining.The heart was harvested and levels of the nuclear factor kappa β(NF-κB)activity were determined by Western Blot,and ultrastructures were observed by electron microscopy.The data was expressed as,and were analyzed by using oneway ANOVA test with SPSS 13.0.P value less than 0.05 indicated statistical significance.Results The NF-κB activity of group S was significantly lower than that of group I/R(P<0.05).Group S significantly(P<0.05)reduced infarct size(19.7%±2.8% in group S) of the left ventricular area at risk as compared with control (37.8 %±1.7 % in I/R group).The injury of I/R group was worse than that of group S from the changes of the cellular structure under light microscope.Group S had a lower levels of TNF-α and also had a higher level of IL-10.Conclusions Isoflurane can inhibit NF-κB activity during myocardial ischemia reperfusion and modulate the cytokine expression,which may be one of molecular mechanisms of Isoflurane delayed preconditioning on cardioprotection.