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目的探讨异氟醚通过抑制细胞间黏附分子(ICAM-1)表达参与减轻肝脏缺血-再灌注(IR)损伤的可能调节机制。方法 32只雌性SD大鼠分为4组。A组大鼠行腹腔注射1%戊巴比妥钠40 mg/kg麻醉,进行手术但不阻断入肝血流;B组1%戊巴比妥钠麻醉后行部分肝脏IR;C组大鼠仅接受1.0 MAC异氟醚吸入麻醉,不阻断血流;D组采用1.0 MAC异氟醚麻醉,建立肝脏IR模型。肝脏缺血60 min,再灌注3 h后取肝组织和血液标本,检测血清丙氨酸转氨酶(ALT)和天冬门氨酸转氨酶(AST)、肝组织ICAM-1和肝组织还原型谷胱甘肽(GSH)、脂质过氧化物丙二醛(MDA)和超氧化物歧化酶(SOD)含量。结果与戊巴比妥钠麻醉比较,采用异氟醚处理后明显降低血清ALT和AST的水平,再灌注肝组织内GSH、SOD含量明显高于而MDA含量降低,同时抑制肝组织ICAM-1的表达。结论异氟醚麻醉能够有效减轻肝脏IR损伤,抑制氧自由基的生成和释放,具体机制可能与抑制ICAM-1表达致使细胞内GSH含量增加密切相关。
Objective To investigate the possible regulatory mechanism of isoflurane on hepatic ischemia-reperfusion injury by inhibiting the expression of intercellular adhesion molecule-1 (ICAM-1). Methods 32 female SD rats were divided into 4 groups. Rats in group A were anesthetized by intraperitoneal injection of 1% sodium pentobarbital 40 mg / kg for surgery but did not block hepatic blood flow. Partial liver IR was performed in group B with 1% pentobarbital sodium anesthesia; group C Rats received 1.0 MAC isoflurane inhalation anesthesia, do not block blood flow; Group D was anesthetized with 1.0 MAC isoflurane to establish the liver IR model. Hepatic ischemia 60 min, 3 h after reperfusion, liver tissue and blood samples were collected to detect serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), liver tissue ICAM-1 and reduced liver tissue (GSH), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. Results Compared with sodium pentobarbital anesthesia, the levels of ALT and AST in serum were significantly decreased after isoflurane treatment. The levels of GSH and SOD in liver tissue were significantly higher than those in pentobarbital sodium group and MDA content was decreased, meanwhile ICAM-1 expression. Conclusion Isoflurane anesthesia can effectively reduce liver IR injury and inhibit the production and release of oxygen free radicals. The specific mechanism may be related to inhibiting the expression of ICAM-1 and increasing the intracellular GSH level.