摘要
目的 :探讨脂肪肝热缺血再灌注损伤过程中丙二醛 ( MDA)、谷丙转氨酶 ( ALT)、内皮素( ET- 1)及肿瘤坏死因子 ( TNFα)的变化。方法 :首先通过给予实验动物改良的缺乏胆碱和蛋氨酸( CMDD)饲料制备脂肪肝模型 ,观察脂肪肝组和正常肝组门脉压的关系 ,以及在缺血前、缺血 15或30 min再灌注 60 min时 ,肝组织中 MDA、血清 ET- 1、TNFα、ALT水平的变化。结果 :脂肪肝组门静脉压高于正常肝组 ,缺血前后脂肪肝组肝组织中 MDA含量以及血清 ET- 1、TNFα、AL T水平高于正常肝组 ,并随缺血时间延长而增高。结论 :肝脂肪变性引起肝窦狭窄和不规则 ,门脉压增高。含大量脂肪的肝细胞对热缺血再灌注损伤敏感性增高 ,通过产生过多的 MDA、ET- 1、TNFα,导致肝细胞破坏 ,血清AL T升高。
Objective:To investigate the changes of MDA,ALT,ET 1 and TNFα during warm ischemia reperfusion injury to liver using a rat fatty liver model.Methods:The rats of fatty liver group were fed with a diet deficient in choline and amino acid (methionine in chief) and fatty liver model was produced successfully.Rat portal vein pressure changes before ischemia,and changes of MDA,ALT,ET 1 and TNFα before ischemia and ischemia for 15 min or 30 min followed by 60 min of reperfusion were observed.Results:Portal vein pressure of fatty liver group was higher than that of normal liver group.The contents of MDA,ALT,ET 1 and TNFα of fatty liver group before and after ischemia were higher than those of normal liver group.Conclusion:Liver steatosis can result in narrow and irregular liver sinus, and increase of portal vein pressure.The liver cells containing many fatty droplets are sensitive to I/R injury.And MDA,TNFα and ET 1 produced from I/R injury make liver cells destroy and ALT increase. [
出处
《白求恩医科大学学报》
CAS
CSCD
北大核心
2001年第3期252-254,共3页
Journal of Norman Bethune University of Medical Science
