摘要
目的 :探讨预处置对缺血再灌注损伤肝脏的防护及其机制。方法 :随机将家兔分为对照组、缺血再灌注组和预处置组 ,复制肝缺血再灌注损伤 (HIRI)模型 ,观察反复 3次缺血 5min再灌注 5min(预处置 )后再缺血 45min再灌注 45min ,对血浆、肝组织一氧化氮 (NO)和丙二醛 (MDA)水平、谷丙转氨酶 (ALT)值及肝细胞形态学改变的影响。结果 :肝缺血再灌注期间 ,预处置组血浆及肝组织NO水平明显高于缺血再灌注组 (P <0 0 5 ) ;而MDA水平和血浆ALT均显著低于缺血再灌注组 (P <0 0 5和P <0 0 1) ;且与仅行游离、不阻断肝血流的对照组比较均无明显差异 ;肝细胞形态学异常改变也明显减轻。结论 :预处置可通过提高体内NO水平及降低体内氧自由基水平而减轻HIRI。
AIM:To investigate the protective effect of preconditioning on rabbit liver during total ischemia and reperfusion and its mechanism. METHODS: Using hepatic ischemia and reperfusion injury (HIRI) model in rabbits, animals were randomly divided into three groups: control group (A), non-preconditioning group(B) and preconditioning group(C), different effects of preconditioning on several parameters including alanine aminotransferase (ALT) activity and levels of nitric oxide (NO) and malondialdehyde (MDA) in plasma or liver tissue as well as hepatocellular morphological changes were measured and observed during HIRI. RESULTS:In C group NO levels of plasma and liver tissue were higher than those in B group (P<0.05);While MDA levels and ALT value in plasma were lower than those in B group (P<0.05 and P<0.01); and there were not significant differences between C and A group (P>0.05); abnormal morphological chages of liver cells in A group were ameliorated remarkably too during HIRI. CONCLUSION:Preconditioning can attenuate HIRI by improving NO level and reducing oxygen free radicals level.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第3期203-206,共4页
Chinese Journal of Pathophysiology
基金
浙江省卫生厅科研基金资助! (No .98A0 87)