Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury

J. H. Eisenach, R. S. Friese, B. C. Sheridan, J. Agrafojo, R. C. McIntyre, A. H. Harken, D. A. Fullerton

Research output: Contribution to journalArticlepeer-review


A major feature of acute lung injury (ALT) is pulmonary vasoconstriction secondary to pulmonary vascular endothelial injury with loss of endothelial-derived nitric oxide (NO). In a rat model of ALI produced by gut ischemia/reperfusion (I/R), our purpose was to examine the effect of exogenous (inhaled) NO on lung neutrophil accumulation (myeloperoxidase, MPO) and 2 modes of endothelial-dependent pulmonary vasorelaxation: (1) receptor-dependent (acetylcholine, ACh) and (2) receptor-independent (A23187). Methods: 5 ventilated rats had gut I/R by superior mesenteric artery occlusion for 1 hr. After 2 hrs of reperfusion, lung MPO was determined. Dose response curves to ACh and A23187 were studied in isolated pulmonary artery rings preconstricted with phenylephrine. NO treated rats (n=5) received inhaled NO (20ppm) for the period of gut I/R. 5 rats had sham laparotomy. Statistics were by ANOVA, *p<0.05. Results: Inhaled NO prevented lung neutrophil accumulation and pulmonary endothelial dysfunction. Conclusion: Inhaled NO prevents pulmonary endothelial dysfunction in ALI.

Original languageEnglish (US)
Pages (from-to)167A
JournalJournal of Investigative Medicine
Issue number1
StatePublished - 1996

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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