A novel nitric oxide scavenger decreases liver injury and improves survival after hemorrhagic shock

John Menezes, Christian Hierholzer, Simon C. Watkins, Valerie Lyons, Andrew B. Peitzman, Timothy R. Billiar, David J. Tweardy, Brian G. Harbrecht*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

79 Scopus citations


We tested the ability of a nitric oxide (NO) scavenger to reduce tissue injury in a rodent model of hemorrhagic shock. Rats were hemorrhaged to a mean arterial blood pressure (MAP) of 40 mmHg and then resuscitated when either 30% of their shed blood had been returned (group 1) or after 100 min of continuous shock (group 2). Selected animals were treated with the NO scavenger NOX (30 mg · kg-1 · h-1) infused over 4 h. Hemorrhaged rats had a lower MAP after resuscitation compared with sham-shock control rats. NOX treatment significantly increased MAP after resuscitation from hemorrhage. Hemorrhagic shock also increased liver injury as reflected by elevated ornithine carbamoyltransferase (OCT) plasma levels, and NOX treatment significantly reduced OCT release. In addition, NOX was associated with significantly decreased hepatic neutrophil infiltration and improved 24- h survival (n = 8 of 9) compared with saline-treated shock animals (n = 3 of 9). These data suggest that excess NO mediates shock-induced tissue injury and that suppression of NO availability with NO scavengers may reduce the pathophysiological sequelae of severe hemorrhage.

Original languageEnglish
Pages (from-to)G144-G151
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number1 40-1
StatePublished - Jul 1999
Externally publishedYes


  • Multiple organ failure
  • Nitric oxide synthase
  • Trauma kidney


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