Tissue oxygen saturation of human hepatic grafts after reperfusion: paradoxical elevation in poor graft function.

The present study investigated the pathophysiology of primary nonfunction (PNF) of grafted livers with regard to hepatic tissue oxygenation. Hemoglobin oxygen saturation in hepatic tissue (H-So2) after reperfusion was determined using near-infrared spectroscopy. Graft tissue oxygen consumption was also estimated according to Fick's principle. Six grafts with PNF were compared with 40 functioning grafts. One PNF graft with extremely low and heterogeneous H-So2 after reperfusion was found to contain multiple intrahepatic portal thrombi. However, five other PNF grafts showed no lower and, on the contrary, more homogeneous H-So2 at the end of the operation. As a whole, mean H-So2 was negatively correlated and the coefficient of variation (CV) of H-So2 was positively correlated with graft tissue oxygen consumption at the end of the operation; grafts whose H-So2 showed a secondary decrease had better initial function. In later relaparotomy, the H-So2 of the five PNF grafts was significantly higher and more homogeneous than that of the functioning grafts. These results suggest that H-So2 level reflects tissue oxygen consumption as well as oxygenation, and that the dissociation of both factors can occur in hepatic graft reperfusion. Not only low and heterogeneous H-So2 but also high and homogeneous H-So2, suggesting some shunt mechanism, can be signs of poor graft function.