Post-ischemic shunt following hepatic ischemia/reperfusion does not affect tissue chemokine levels or tissue injury

Hepatic ischemia followed by reperfusion causes the release of a cascade of mediators, including tumor necrosis factor-ct and epithelial neutrophil activating protein (ENA-78), which are important in the subsequent development of the lung and liver injury associated with this insult. We hypothesize that preferential post-ischemic shunting of blood into the nonischemic hepatic lobes at the time of reperfusion may increase the ischemic injury. To test this hypothesis, we utilized a rat model of lobar no-flow hepatic ischemia/reperfusion and removed the nonischemic hepatic robes at the time of reperfusion to eliminate the preferential shunting of blood into the nonischemic tissues. We assessed pulmonary and hepatic tissue levels of ENA-78, pulmonary neutrophil influx and changes in pulmonary capillary permeability, and liver injury as measured by hepatic neutrophil influx and serum transaminase levels. Our results demonstrated that there were no significant differences in pulmonary and hepatic levels of ENA-78, or in the development of the lung and liver injury in animals undergoing resection of the nonischemic hepatic lobes at the time of reperfusion, as compared with animals undergoing hepatic ischemia/reperfusion alone.