论文部分内容阅读
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 liver ischemia / reperfusion injury and its mechanism at room temperature. Methods 24 rabbits were randomly divided into ischemia group and control group. Tissue gas analyzer continued to measure the hepatic tissue oxygen tension (HepatictissueoxygeonpressurePtiO2); light and electron microscopy pathological changes of liver tissue; automatic biochemical analyzer serum alanine aminotransferase (ALT). Results The PtiO2 of the liver of ischemic group began to decrease after ischemia, decreased to 2101 ± 28 after 30min, the value of PtiO2 began to recover after reperfusion, and returned to normal at 60min after reperfusion (P <0 0 5). Hepatic cells degeneration, necrosis, serum ALT increased significantly, the most serious in the liver reperfusion 60min. Conclusion Progn’s blockade of hepatic blood flow at room temperature leads to hepatic dysfunction and pathological changes following hepatic ischemia / reperfusion. Its mechanism of action is related to ischemia hepatocyte hypoxia, liver microcirculation disturbance and hepatocyte mitochondria damage during reperfusion period.