The roles of iNOS in liver ischemia-reperfusion injury

Vincent G. Lee, Mark L. Johnson, Jeffrey Baust, Victor E. Laubach, Simon C. Watkins, Timothy R. Billiar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

105 Scopus citations


To determine the contribution of the inducible nitric oxide synthase (iNOS) to hepatic injury following warm ischemia-reperfusion, we developed a model of partial hepatic ischemia-reperfusion in mice and studied the injury response in iNOS knockout (KO) mice. Compared with wild types, iNOS KO animals exhibited lower plasma transaminase levels after 1 and 6 h of reperfusion following 1 h of ischemia. At the 3-h time point, enzyme levels were not different between the two groups. iNOS mRNA was not detectable in the ischemic hepatic lobes of wild-type mice until 3 h of reperfusion; however, perfusion studies identified a significant delay in reperfusion of the ischemic lobe in the iNOS KO mice at the 1-h time point with similar perfusion rates at 3 and 6 h compared with wild type. By way of comparison, mice deficient in the endothelial NOS (eNOS) were also assessed for the degree of hepatic damage 3 h post-reperfusion. Plasma transaminase levels were significantly increased in eNOS KO animals compared with wild-type controls. These data suggest that systemic as well as local sources of iNOS regulate reperfusion, and local iNOS contributes to hepatic injury, while eNOS is protective in warm hepatic ischemia-reperfusion.

Original languageEnglish
Pages (from-to)355-360
Number of pages6
Issue number5
StatePublished - Nov 2001
Externally publishedYes


  • Ischemia-reperfusion
  • Liver
  • Nitric oxide
  • Nitric oxide synthase


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