异氟烷对大鼠肝脏缺血再灌注损伤时细胞间黏附分子-1表达的影响

目的研究异氟烷对大鼠肝脏缺血再灌注损伤后细胞间黏附分子-1（ICAM-1）的影响，探讨异氟烷肝脏缺血再灌注保护作用的机制。方法将32只SD成年雌性大鼠分为假手术组、缺血再灌注组、异氟烷组、异氟烷．缺血再灌注组。假手术组、异氟烷组作为对照；缺血再灌注组和异氟烷-缺血再灌注组阻断支配大鼠肝脏左叶和中叶的门静脉分支，建立肝脏70％缺血再灌注模型，缺血60min再灌注3h后取材，测定大鼠血清ALT、AST；免疫组织化学方法检测ICAM-1蛋白的表达，HE染色进行病理学检查。结果肝脏缺血60min再灌注3h后肝组织ICAM-1蛋白表达水平增高；血清酶ALT和AST升高；肝组织损害严重。异氟烷抑制ICAM-1表达，降低ALT、AST水平，减轻肝细胞损伤。结论肝脏缺血再灌注损伤程度与肝组织内ICAM-1水平有密切的关系，异氟烷可抑制肝脏缺血再灌注期间肝组织ICAM-1的表达，同时减轻伤肝脏损伤。

Effect of Isoflurane on ICAM-1 expression in rats during liver ischemia-reperfusion injury

Objective To investigate the role of intercellular adhesion molecule-1(ICAM-1)in Isoflurane against hepatic ischemia-reperfusion(I/R)injury in vivo.Methods Thirty-two female SD rats were randomly divided into 4 groups:sham-operation group(A),I/R group(B),Isoflurane group(C),I/R Isoflurane group(D).Groups A and C were be used as controls.In groups B and C,the hepatic hilar vessels distributing to the left and median lobes were clamped to induce partial hepatic ischemia(70%).Reperfusion was done 60 min after hepatic ischemia.The animals were killed 3 h after reperfusion,then the specimens of liver tissues and blood were obtained.ALT and AST in blood serum were detected as liver damage markers.The histological examination of liver tissues was done by hematoxylin and eosin staining.The levels of ICAM-1 protein in the hepatic tissues were detected by immunohistochemistry.Results After hepatic ischemia-reperfusion,the ICAM-1 protein expression in the hepatic tissues increased;ALT and AST increased;Reperfusion induced severe liver damage.Isoflurane significantly inhibited the ICAM-1 expression.Conclusion The degree of hepatic ischemia-reperfusion injury is closely associated with the expression level of ICAM-1.Isoflurane abates liver ischemia-reperfusion injury and inhibits the ICAM-1 expression.