The aim of this study is to assess ischemia/reperfusion injury in carbon tetrachloride induced cirrhotic liver as compared to normal liver in the rats. Results showed that in cirrhotic liver, instead of diminishing the hepatic vein nitric oxide level increased significantly after ischemia from 8.04 μmol/L to 11.52 μmol/L and remained high till 5 hrs after reperfusion. The hepatic adenosine triphosphate (ATP) contents decreased as that seen in normal rat but did not restore to normal till the end of 5 hrs after reperfusion. Based on these findings, it is postulated that in cirrhotic liver, ischemia/reperfusion injury is aggrvated as evidenced by of nitric oxide, and extended diminishing in ATP.
