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Am J Physiol Gastrointest Liver Physiol 284: G536-G545, 2003. First published November 20, 2002; doi:10.1152/ajpgi.00400.2002
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Vol. 284, Issue 3, G536-G545, March 2003

Regulation of postischemic liver injury following different durations of ischemia

Ian N. Hines1, Jason M. Hoffman1, Heleen Scheerens2, Brian J. Day3, Hirohisa Harada1, Kevin P. Pavlick1, Sulaiman Bharwani4, Robert Wolf5, Bifeng Gao6, Sonia Flores6, Joe M. McCord6, and Matthew B. Grisham1

Departments of 1 Molecular and Cellular Physiology, 4 Pediatrics, and 5 Medicine, LSU Health Sciences Center, Shreveport, Louisiana 71130; 2 DNAX Research Institute, Palo Alto, California 94304; 3 National Jewish Medical and Research Center, Denver 80206; and 6 Webb-Waring Institute, University of Colorado Health Sciences Center, Denver, Colorado 80262

The objective of this study was to define the relationship among Kupffer cells, O<UP><SUB>2</SUB><SUP>−</SUP></UP> production, and TNF-alpha expression in the pathophysiology of postischemic liver injury following short and long periods of ischemia. Using different forms of superoxide dismutase with varying circulating half-lives, a monoclonal antibody directed against mouse TNF-alpha , and NADPH oxidase-deficient mice, we found that 45 or 90 min of partial (70%) liver ischemia and 6 h of reperfusion (I/R) produced time-dependent increases in liver injury and TNF-alpha expression in the absence of neutrophil infiltration. Furthermore, we observed that hepatocellular injury induced by short periods of ischemia were not dependent on formation of TNF-alpha but were dependent on Kupffer cells and NADPH oxidase-independent production of O<UP><SUB>2</SUB><SUP>−</SUP></UP>. However, liver injury induced by extended periods of ischemia appeared to require the presence of Kupffer cells, NADPH oxidase-derived O<UP><SUB>2</SUB><SUP>−</SUP></UP>, and TNF-alpha expression. We conclude that the sources for O<UP><SUB>2</SUB><SUP>−</SUP></UP> formation and the relative importance of TNF-alpha in the pathophysiology of I/R-induced hepatocellular injury differ depending on the duration of ischemia.

transplantation; leukocytes; reactive oxygen species; proinflammatory cytokines; NADPH oxidase


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