Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury

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

Research output: Contribution to journalArticle

Abstract

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)
JournalJournal of Investigative Medicine
Volume44
Issue number1
StatePublished - 1996
Externally publishedYes

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Acute Lung Injury
Nitric Oxide
Lung
Rats
Reperfusion
Calcimycin
Peroxidase
Acetylcholine
Neutrophils
Ischemia
Phenylephrine
Analysis of variance (ANOVA)
Superior Mesenteric Artery
Vascular System Injuries
Lung Injury
Cholinergic Receptors
Vasoconstriction
Vasodilation
Laparotomy
Pulmonary Artery

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Eisenach, J. H., Friese, R. S., Sheridan, B. C., Agrafojo, J., McIntyre, R. C., Harken, A. H., & Fullerton, D. A. (1996). Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury. Journal of Investigative Medicine, 44(1).

Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury. / Eisenach, J. H.; Friese, Randall S; Sheridan, B. C.; Agrafojo, J.; McIntyre, R. C.; Harken, A. H.; Fullerton, D. A.

In: Journal of Investigative Medicine, Vol. 44, No. 1, 1996.

Research output: Contribution to journalArticle

Eisenach, JH, Friese, RS, Sheridan, BC, Agrafojo, J, McIntyre, RC, Harken, AH & Fullerton, DA 1996, 'Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury', Journal of Investigative Medicine, vol. 44, no. 1.
Eisenach JH, Friese RS, Sheridan BC, Agrafojo J, McIntyre RC, Harken AH et al. Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury. Journal of Investigative Medicine. 1996;44(1).
Eisenach, J. H. ; Friese, Randall S ; Sheridan, B. C. ; Agrafojo, J. ; McIntyre, R. C. ; Harken, A. H. ; Fullerton, D. A. / Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury. In: Journal of Investigative Medicine. 1996 ; Vol. 44, No. 1.
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