Does upregulation of inducible nitric oxide synthase play a role in hepatic injury?

Terrence H. Liu, Emily K. Robinson, Kenneth S. Helmer, Sonlee D. West, Antonio A. Castaneda, Lily Chang, David W. Mercer

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Lipopolysaccharide (LPS) and gut ischemia/reperfusion (I/R) injury cause reversible liver injury. Because nitric oxide (NO) can have both beneficial and deleterious effects in the gastrointestinal tract, and because the role of NO in gut I/R-induced hepatic injury is unknown, this study examined its role in LPS and gut I/R-induced hepatic injury in the rat. Both LPS and gut I/R caused a similar increase in serum hepatocellular enzymes. LPS but not gut I/R caused a significant increase in upregulation of hepatic inducible NO synthase (iNOS) according to quantitative real-time RT-PCR and Western immunoblot analysis. Aminoguanidine, a selective iNOS inhibitor, attenuated LPS-induced hepatic injury and hypotension, but did not prevent gut I/R-induced hepatic injury. In contrast, the non-selective NOS inhibitor NG-nitro-L-arginine methyl ester aggravated liver damage from both LPS and gut I/R. These data indicate that iNOS plays a role in mediating LPS-induced hepatic injury, but not gut I/R-induced hepatic injury. The data also suggest that the constitutive isoforms of NOS play a hepatoprotective role in both models of hepatic injury.

Original languageEnglish (US)
Pages (from-to)549-554
Number of pages6
Issue number6
StatePublished - Dec 2002
Externally publishedYes


  • Aminoguanidine
  • Constitutive nitric oxide synthase
  • Gut ischemia/reperfusion
  • Lipopolysaccharide
  • N-nitro-L-arginine methyl ester

ASJC Scopus subject areas

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine


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