Abstract:Objective:To study the injurious effect of active oxygen on hepatocarcinoma after ischemia and reperfusion.
Methods :The models of ischemia and reperfusion（I/R） of hepatocarcinoma were established. The model was reperfued alone or combination with perfued with hyperoxic fluid（Partial pressure of oxygen, PO2 >80) via portal vein. After reperfusion 1 h, 1 d, 3d and 7 d respectively, the concentration of superoxide dismutase（SOD） and catalase (CAT) were tested, and the apoptosis of hepatocarcinoma also was observed using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method.
Results:The results indicated that the SOD concentration in both hepatocarcinoma tissue and normal hepatic tissues decreased following I/R and perfusion with hyperoxic fluid liquid.The concentration of CAT increased following I/R in normal hepatic tissues.In hepatocarcinoma tissue, concentration of CAT decreased after reperfusion for 1 d and reached its lowest point. After perfusion with hyperoxic fluid,the concentration of SOD in both hepatocarcinoma tissue and normal hepatic tissues decreased more quickly following I/R and the low level was still found on 7 d after reperfusion. The concentration of CAT in tissues of both groups decreased and reached the lowest level at 1 h after reperfusion, but it was restored at 3 d reperfusion in normal hepatic tissues, and in hepatocarcinoma tissue was still at lower level until 7 d after reperfusion. After I/R, the apoptotic cells increased in normal hepatic and hepatic cancer tissues, and were most marked in tissues of hepatic carcinoma at 1 d and 3 d after perfusion with hyperoxic fluid. After I/R and perfusing with hyperoxic fluid, the changes of SOD and CAT and apoptosis in hepatocarcinoma tissue were more obvious than that in normal hepatic tissues（P<0.01）.
Conclusions:Perfusion with hyperoxic fluid via portal vein can intensify hepatio ischemia and reperfusion injury, but has less effect on normal hepatic tissues.