RESUMO
A rat liver normothermic ischemia-reperfusion model was used to investigate whether hypoxanthine (HXA) that accumulated during ischemia was washed out in hepatic veins during reperfusion. Ischemia was induced in median and left lobes by clamping of the proper hepatic artery and portal branches. The effect of allopurinol (ALL) on metabolism of ATP and HXA was studied before, during and after a 60-min normothermic ischemic insult. Liver cell concentration of HXA in the group treated with ALL increased during ischemia and decreased rapidly during the first 10-min reperfusion. Recovery of ATP increased gradually during the 10-min reperfusion period and was significantly higher in the group treated by ALL compared to that of controls. Liver venous blood concentration of HXA in the ALL-treated group was 10-to 40-fold lower than that in liver tissue. The rapidly decreasing concentration of HXA in liver tissue during reperfusion and a minimal washout may indicate that HXA was used for resynthesis of ATP during reperfusion.
