常温下肝脏缺血/再灌注损伤及其机制的实验研究  

Experimental study of injure and its mechanism in the ischemia and reperfusion period in rabbit liver

作　　者：王成友[1] 倪勇[1] 何海萍[1] 刘琰[2] 

机构地区：[1]广东深圳市第二人民医院肝胆外科,518035 [2]广东深圳市第二人民医院中心实验室,518035

出　　处：《中国基层医药》2003年第3期196-197,共2页Chinese Journal of Primary Medicine and Pharmacy

摘　　要：目的　研究常温下肝脏缺血 /再灌注损伤及其机制。方法　 2 4只兔随机均分为缺血组和对照组。组织气体分析仪持续测定兔肝组织氧压 (HepatictissueoxygeonpressurePtiO2 ) ;光镜及电镜观察肝脏组织病理改变 ;全自动生化仪测定血清丙氨酸氨基转氨酶 (ALT)。结果　缺血组兔肝脏在缺血后肝PtiO2 值开始下降、30min降至 2 0 1± 2 8,再灌注后的肝PtiO2 值开始恢复 ,再灌注 6 0min肝PtiO2 未恢复正常 (P <0 0 5 )。肝细胞出现变性、坏死 ,血清ALT值显著升高 ,在肝脏再灌注 6 0min时最为严重。结论　常温下用Pringle氏法阻断入肝血流可导致肝脏缺血/再灌注后肝细胞功能障碍和病理损害。其作用机制与缺血期肝细胞缺氧、再灌注期肝脏微循环障碍和肝细胞线粒体的损伤有关。Objective To study the injury a nd its mechanism in the ischemia and reperfusion period in rabbit liver. Methods Twenty four rabbits were randomly divided into the ischemia an d reperfusion group and normal control group.Hepatic tissue oxygeon pressure(P ti O 2) was measured before,during,and after the ischemic period in the left lobe.Plasma glutamic pyruvic transaminase enzyme(ALT) was also measured.The hi stopathologic alteration of the liver was observed.Results ALT and P ti O 2 value in the ischemia and reperfusion group at liver ischemia reperfusion different periods remained significantly higher than that in the c ontrol group(P<0.05).Meanwhile,the histopathologic injury of li ver were significantly remarkable in the ischemia reperfusion group.Con clusion The liver ischemia reperfusion injury may be induced by Pringl e maneuver.The mechanism is associated with cell anoxia,the disorder of microcir culation and injury of mitochodria of hepatic cells during ischemia.

关 键 词：实验研究 缺血再灌注 氧压 肝损伤 

分 类 号：R363[医药卫生—病理学]