Isoflurane preconditioning decreases the plasma concentration of matrix metalloproteinase-9 and protects myocardium against cardiopulmonary bypass in cardiac valve replacement / 中南大学学报(医学版)

OBJECTIVE@#To explore the effect of isoflurane preconditioning on the plasma concentration of matrix metalloproteinase (MMP)-9 and myocardial ultramicrostructure in patients undergoing cardiac valve replacement.@*METHODS@#Thirty patients undergoing elective cardiac valve replacement with cardiopulmonary bypass (CPB) were randomly assigned to a control group (ný15) and an isoflurane group (ný15). In the isoflurane group, isoflurane of 1.0 minimum alveolar concentration end-tidal( 1.1% approximately 1.2%) was administered for 30 min followed by a 15 min washout period before the CPB. The control group did not inhale isofurane, and there was no difference in the other drugs in the 2 groups. Blood samples for MMP-9 were obtained before incision(T(0)) and at 30 min (T(1)),6 h (T(2)),12 h (T(3)), and 24 h (T(4)) after the reperfusion. Right atrial biopsies were collected before and after the CPB to observe the myocardial ultramicrostructure.@*RESULTS@#Compared with T(0), the mean MMP-9 level significantly increased at T(1), T(2) and T(3) in the control group(P<0.01), while the MMP-9 level only at T(1) significantly increased in the isoflurane group (P<0.01). The mean MMP-9 level was significantly reduced in the isoflurane group at T(2) compared with each time point in the control group. The difference in MMP-9 levels between T(1), T(2), T(3) and T(0) was significantly lower in the isoflurane group than that in the control group (P<0.01). The ultramicrostructure injury of myocardium under electron microscope in the control group was worse than that in the isoflurane group.@*CONCLUSION@#The plasma concentration of MMP-9 is inhibited by isoflurane preconditioning in patients undergoing cardiac valve replacement after CPB, which might be part of its protective mechanism against myocardium injury after CPB.

Effects of isoflurane delayed preconditioning on nuclear factor-κB during myocardial ischemia reperfusion injury in rabbits / 中华急诊医学杂志

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.