The liver is an organ with abundant blood flow, consisting of hepatic arterial and portal blood flow. The viability of liver tissue depends on the condition of the hepatic microcirculation which is controlled by hepatic sinusoidal lining cells. Hepatic ischemia and reperfusion (HIR) injury is inevitable in surgical procedures for liver trauma and hepatectomy as well as liver transplantation. Reperfusion through an ischemically damaged organ enhances the tissue injury. Cytokines are pivotal factors in neutrophil-mediated liver injury following HIR, while various other mediators are involved in this insult. Advances in molecular biology have allowed the identification of various cytokines. Inflammatory cytokines such as TNF-alpha are associated with the induction of cellular adhesion molecules and hepatic microcirculatory impairment based on neutrophil-vascular endothelial cell interaction. Members of the chemokine family such as IL-8, CINC, MIP-2, and MCP-1 are involved in neutrophil infiltration in the liver and remote organs. Since each cytokine has a wide variety of actions and interacts' among others' via the cytokine network, their actions in HIR injury have not been determined completely. Kupffer cells have been focused on as a source of cytokine production in HIR injury. Further studies on the mechanisms of cytokine production after HIR and analysis of regulation in the cytokine network would clarify the pathophysiology of HIR injury and the most suitable therapeutic strategy for this insult.