Effects Of Sevoflurane Preconditioning On Expression Of TNF-α And ICAM-1 In Ischemia-Reperfused Rat Myocardium

ObsjectiveTo investigate the myocardial infarct size and effect of sevoflurane preconditioning on myocardium expression of TNF-αand ICAM-1 in ischemia-reperfused rats.MethodsMyocardial ischemia-reperfusion injury model was instrumented in rats.Forty male SD rats, weighing 270-350g were anesthetized. Sixteen animals were randomly divided into 2 groups of 8 animals each:(C)I/R group and (D)SEVO+I/R group. At the end of 2h reperfusion the size of myocardial infarct was determined using triphenyltetrazolium chloride staining. Another twenty-four male SD rats were randomly divided into four groups of 6 animals each:: (A) CON group:control group without LCA occlusion;(B) SEVO group:inhaled 1.0 MAC sevoflurane 30min and 165min wash-out;(C)I/R group:Rats experienced myocardium ischemia-reperfusion merely;(D) SEVO+I/R group:Rats received 1.0 MAC sevoflurane for 30 min and 15 min wash-out ,followed by 30 min of left coronary artery occlusion and 2h of reperfusion. At the end of 2h of reperfusion.myocardial specimens were obtained for determination of expression of TNF-αand ICAM-1 protein in myocardium (by Western blot).ResultsThere was no statistically significant difference in HR, MAP and RPP among all groups during the baseline (P>0.05). During 30 minutes of sevoflurane administering, there was statistically significant difference in HR, MAP and RPP among group B and group D (P<0.05) 1h and 2h after reperfusion, there was significant difference in MAP and RPP among group C and group D(P<0.05). Infarct size in group D was significantly (P<0.05) reduced (36.82±4.99%) compared with group C(52.48±6.04%) (P<0.05). The expression of TNF-αand ICAM-1 protein was up-regulated in group C and group D as compared to group A.The expression of TNF-αand ICAM-1 protein was significantly higher in group D than group C.ConclusionSevoflurane preconditioning can reduce myocardial infarct size in rats to some extent and protect the heart against ischemia-reperfusion injury by inhibiting the protein expression of TNF-αand ICAM-1.