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.