Ischaemia-Reperfusion Injury and Liver Transplantation

Chemiluminescence has been used to show increased free-radical production in I/R injury in isolated hepatocytes and in isolated rat livers (Caraceni et al., 1992 Nunes et al., 1992). Studies in isolated rat liver have shown that ischaemia results in increased conversion of 

This correlated with a 64% decrease in endogenous hepatic xanthine dehydrogenase/oxidase activity. 

A number of studies have demonstrated the depletion of antioxidants during ischaemia. SOD and hepatic GSH are decreased after periods of ischaemia or haemorrhagic shock (Shi et al., 1986 Younes and Strubelt, 1988 Marubayashi et al., 1989 Stein et al., 

Furthermore, depletion of hepatic GSH induced chemically or by fasting augmented hepatic I/R-induced enzyme release and promoted lipid peroxidation (Jennische, 1984 Stein et al., 1991) Benoit et al. (1992) have used portacaval-shunted rats as a model of chronic hepatic ischaemia, and were able to show decreases in total levels of SOD and xanthine dehydrogenase, but no significant change in catalase or glutathione peroxidase. 

The effects of ROM on liver have already been discussed. The potential involvement of ROM in I/R injury is suggested by the finding that glycogen-depleted livers are more susceptible to ischaemic injury. This is thought to be related to accumulation of hypoxanthine during anaerobic metabolism, which serves as a substrate for XO and hence enhanced production of RDM (Younes and Strubelt, 1988). 

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