摘要
目的 :探讨缺血后处理对肝脏缺血再灌注损伤的保护作用。方法 :建立大鼠肝脏局部缺血再灌注模型 ,将 32只健康雄性Wistar大鼠随机分为假手术、缺血再灌注、腺苷处理及缺血后处理 4组 ,分别于缺血 6 0min恢复全面血液再灌前 ,先经门静脉缓慢推注外源性腺苷 ,或先给予反复短暂的预再灌、停灌作缺血后处理 ,观察血清肝酶、透明质酸 (HA)水平及肝组织中丙二醛 (MDA)、超氧化物歧化酶 (SOD)、一氧化氮 (NO)、内皮素 1(ET 1)的含量变化 ,并行肝组织病理学检查。结果 :与缺血再灌注组相比 ,缺血后处理组肝酶的漏出、血清HA水平及肝组织MDA、ET 1含量明显降低 (P <0 .0 1) ,而SOD、NO含量则显著升高 (P <0 .0 1) ,同时肝组织病理形态学损伤亦明显减轻 ,而腺苷处理组与缺血再灌注组相比无显著性差异 (P >0 .0 5 )。结论 :缺血后处理可通过抑制再灌注后氧自由基的过量生成 ,改善肝脏微循环 ,发挥保护效应。
Objective: To investigate the protective effect of ischemic postconditioning (IPo) on hepatic ischemia-reperfusion injury in rats. Methods:With a rat model of acute liver ischemia-reperfusion,32 healthy male Wistar rats were randomly divided into sham-operated,ischemia-reperfusion (IR),adenosine-conditioning and IPo group. Before persistent reperfusion, adenosine-conditioning was achieved by injection of adenosine through portal vein,while in IPo group,animals were given several brief reperfusion-ischemia. The sample of blood and hepatic tissue of all groups were taken after experiment. Results: Compared with IR group,the activity of plasma enzyme and hyaluronic acid (HA) and the concentrations of malondialdehyde (MDA) and endothelin-1 (ET-1) in hepatic tissue in IPo group decreased markedly(P<0.01),while the concentrations of superoxide dismutase (SOD) and nitric oxide (NO)increased significantly(P<0.01). Moreover,the hepatic congestion and pathological damage also relieved obviously. But the difference between adenosine-conditioning and IR group was not significant(P>0.05). Conclusion: IPo can reduce the synthesis of oxygen free radicals after reperfusion to improve hepatic microcirculation and,consequently,can attenuate hepatic ischemia-reperfusion injury.
出处
《武汉大学学报(医学版)》
CAS
2004年第2期104-107,共4页
Medical Journal of Wuhan University
关键词
肝脏
缺血再灌注损伤
缺血后处理
微循环
liver
ischemia-reperfusion injury
ischemic postconditioning
microcirculation