肝硬变大鼠肝脏缺血再灌注损伤

为比较硬化肝与正常肝在缺血再灌注损伤时的差异和意义。作者采用四氯化碳复制大鼠肝硬变模型,通过大鼠肝脏缺血再灌注损伤模型,检查不同时限大鼠门静脉血内毒素、肝静脉血一氧化氮。结果显示：肝硬变大鼠再灌注时门静脉内毒素水平更高;肝脏ＮＯ合成释放显著增加。作者认为肝硬变时对缺血再灌注损伤反应与正常大鼠不同,可能是肝硬变时对缺血再灌注损伤更敏感,更易发生肝功能衰竭的重要原因。

The hepatic ischemia/reperfusion injury in cirrhotic rats

We assessed ischemia/reperfusion injury in carbon tetrachloride induced cirrhotic liver as compared to normal liver in the rats. Hepatic vein nitric oxide (NO) level was measured by method of luminol chemiluminensence, and portal vein endotoxin level by limulus lysate with chyomogenic substract. In cirrhotic liver, instead of diminishing the hepatic vein NO level increased significantly after ischemia and remained high till 5 hrs postreperfusion. The portal vein endotoxin level was also increased but to a higher level than that of normal liver. In cirrhotic liver, ischemia/reperfusion injury is aggrevated as evidenced by higher level of endotoxin, increased generation of NO.