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The effect of inhaled nitric oxide on smoke inhalation injury in an ovine model.

Abstract
Smoke inhalation is a significant comorbid factor in thermal trauma. The effect of inhaled nitric oxide (NO) on smoke inhalation injury was evaluated in an ovine model. Following smoke exposure, group 1 animals (n = 9) spontaneously breathed room air, and group 2 animals (n = 8) breathed 20 parts per million of NO in air for 48 hours. Cardiopulmonary variables and blood gases were serially measured; bronchoalveolar lavage (BAL) was performed and wet-to-dry lung weight ratios (W/D) determined at 48 hours. Pulmonary vasoconstriction following smoke inhalation was significantly attenuated by inhaled NO (p < 0.05), which exerted no apparent effect on the systemic circulation. In group 2, the serial decline in pulmonary oxygenation was less than in group 1, consistent with a smaller physiologic shunt (p < 0.05). There were no significant differences in W/D, lung compliance, BAL fluid analysis results, or histologic evaluation findings between the two groups. These results suggest that inhaled NO exerted beneficial effects on pulmonary arterial hypertension and oxygenation following smoke inhalation without apparent amelioration of airway inflammation.
AuthorsH Ogura, W G Cioffi Jr, B S Jordan, C V Okerberg, A A Johnson, A D Mason Jr, B A Pruitt Jr
JournalThe Journal of trauma (J Trauma) Vol. 37 Issue 2 Pg. 294-301; discussion 301-2 (Aug 1994) ISSN: 0022-5282 [Print] United States
PMID8064931 (Publication Type: Journal Article)
Chemical References
  • Nitric Oxide
Topics
  • Administration, Inhalation
  • Animals
  • Blood Gas Analysis
  • Bronchi (pathology)
  • Bronchoalveolar Lavage Fluid (chemistry)
  • Hypertension, Pulmonary (physiopathology)
  • Lung (pathology)
  • Male
  • Nitric Oxide (administration & dosage, therapeutic use)
  • Organ Size
  • Sheep
  • Smoke Inhalation Injury (drug therapy, pathology, physiopathology)
  • Trachea (pathology)
  • Vasoconstriction (drug effects)

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