Kupffer cell function in ischemic and nonischemic livers after hepatic partial ischemia/reperfusion

Hepatic partial ischemic/reperfusion (I/R) injury, in which ischemic and nonischemic areas of the liver are likely to respond to each other after reperfusion, often occurs following hepatobiliary surgical procedures. Kupffer cells (KCs) are considered to play a major role in hepatic I/R injury. To study the activation of KCs in ischemic and nonischemic liver tissues following hepatic I/R, we investigated the superoxide generation and proinflammatory cytokine production of KCs in both liver parts in a rat model of partial hepatic I/R injury. KC superoxide generation in the ischemic and nonischemic lobes was upregulated 6 and 24 h after reperfusion, respectively, and then accelerated. The production of interleukin-1 beta (IL-1 beta) by KCs in the ischemic lobes increased during the early and late phases, 6 h and 4S-72h after reperfusion, respectively. A late increase in IL-1 beta production was also observed in the nonischemic lobes. Production of tumor necrosis factor-alpha (TNF-alpha) increased 6-24 h after reperfusion in both lobes. Upregulation of IL-1 beta mRNA in the ischemic lobes preceded the upregulation of TNF-alpha. mRNA in both lobes. The hepatic partial I/R process results in activation of KCs in ischemic and nonischemic areas of the liver. The KCs are activated during the early phase after reperfusion in the ischemic areas, followed by activation in both the ischemic and nonischemic areas. This could be a cause oliver dysfunction after partial hepatic I/R during surgery.