Nitric oxide decreases lung injury after intestinal ischemia

Lance S. Terada, Nancy N. Mahr, Eugene D. Jacobson

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


After injury to a primary organ, mediators are released into the circulation and may initiate inflammation of remote organs. We hypothesized that the local production of nitric oxide (NO) may act to limit the spread of inflammation to secondarily targeted organs. In anesthetized rats, 30 min of intestinal ischemia followed by 2 h of reperfusion (I/R) did not increase lung albumin leak. However, after treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), intestinal I/R led to increased lung leak, suggesting a protective effect of endogenous NO. The site of action of NO appeared to be the lung and not the gut because 1) after treatment with L-NAME, local delivery of NO to the lung by inhalation abolished the increase in intestinal UR-induced lung leak; 2) L-NAME had no effect on epithelial permeability (51Cr-labeled EDTA clearance) of reperfused small bowel; and 3) after treatment with L-NAME, local delivery of NO to the gut by luminal perfusion did not improve epithelial permeability of reperfused intestines. Furthermore, L-NAME increased, and inhaled NO decreased, the density of lung neutrophils in rats subjected to intestinal UR, and treatment with the selectin antagonist fucoidan abolished L-NAME-induced lung leak in rats subjected to intestinal UR. We conclude that endogenous lung NO limits secondary lung injury after intestinal I/R by decreasing pulmonary neutrophil retention.

Original languageEnglish (US)
Pages (from-to)2456-2460
Number of pages5
JournalJournal of applied physiology
Issue number6
StatePublished - Dec 1996


  • acute respiratory distress syndrome
  • inflammation
  • multiorgan failure
  • neutrophils
  • xanthine oxidase

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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