ABSTRACT
Extensive mechanistic investigations have brought considerable progress in our understanding of the pathophysiology of acute liver failure initiated by hepatic ischemia and reperfusion. The liver can be traumatized directly by ischemia-reperfusion, sepsis, viral infection or chemical-induced liver injury. This chapter focuses on pathophysiological events that are initiated by ischemia and are then continued and amplified during reperfusion leading to severe liver injury and acute liver failure. Potential targets for therapeutic interventions in reperfusion injury are the inflammatory mediators responsible for activation of neutrophils and Kupffer cells. Initial effort to study inflammatory mediators in reperfusion injury focused on complement, since there was evidence for a contribution of complement factors to myocardial ischemia/reperfusion injury. The molecular mechanism of cell injury remains one of the most controversial topics in the pathophysiology of reperfusion injury. If reactive oxygen species are generated, it is generally assumed that lipid peroxidation is involved in the injury process.
