title: Nitric oxide inhalation increases alveolar gas exchange by decreasing deadspace volume.
abstract: OBJECTIVE
  To test the hypothesis that nitric oxide inhalation facilitates CO2 elimination by decreasing alveolar deadspace in an ovine model of acute lung injury.
  
  
  METHODS
  Prospective, placebo-controlled, randomized, crossover model.
  
  
  METHODS
  University research laboratory.
  
  
  METHODS
  Eleven mixed-breed adult sheep.
  
  
  METHODS
  To induce acute lung injury, hydrochloric acid was instilled into the tracheas of paralyzed sheep receiving controlled mechanical ventilation. Each sheep breathed 0 ppm, 5 ppm, and 20 ppm nitric oxide in random order.
  
  
  RESULTS
  Estimates of alveolar deadspace volumes and arterial-to-end tidal CO2 partial pressure differences were used as indicators of CO2 elimination efficiency. At a constant minute ventilation, nitric oxide inhalation caused dose-independent decreases in Paco2 (p <.05), alveolar deadspace (p <.01), and arterial-to-end tidal CO2 partial pressure differences (p <.01). We found that estimates of arterial-to-end tidal CO2 partial pressure differences may be used to predict alveolar deadspace volume (r2 =.86, p <.05).
  
  
  CONCLUSIONS
  Estimates of arterial-to-end tidal CO2 partial pressure differences are reliable indicators of alveolar deadspace. Both values decreased during nitric oxide inhalation in our model of acutely injured lungs. This finding supports the idea that nitric oxide inhalation facilitates CO2 elimination in acutely injured lungs. Future studies are needed to determine whether nitric oxide therapy can be used to reduce the work of breathing in selected patients with cardiopulmonary disorders.
authors.affiliation: Department of Pediatrics, University of Florida College of Medicine, Health Science Center, Gainesville, FL 32610-0296, USA. skimmjw@ufl.edu
authors.forename: J W
authors.initials: JW
authors.lastname: Skimming
authors.forename: M J
authors.initials: MJ
authors.lastname: Banner
authors.forename: H K
authors.initials: HK
authors.lastname: Spalding
authors.forename: M J
authors.initials: MJ
authors.lastname: Jaeger
authors.forename: D J
authors.initials: DJ
authors.lastname: Burchfield
authors.forename: P W
authors.initials: PW
authors.lastname: Davenport
mesh_terms: D000280:Administration, Inhalation; D000704:Analysis of Variance; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism*; D018592:Cross-Over Studies; D004195:Disease Models, Animal; D006439:Hemodynamics; D006851:Hydrochloric Acid; D008168:Lung / Q000378:metabolism; D055370:Lung Injury; D009569:Nitric Oxide / Q000008:administration & dosage / Q000494:pharmacology*; D011650:Pulmonary Alveoli / Q000378:metabolism*; D011659:Pulmonary Gas Exchange / Q000187:drug effects*; D011897:Random Allocation; D012126:Respiratory Dead Space; D012756:Sheep
chemical_list: D002245:Carbon Dioxide; D009569:Nitric Oxide; D006851:Hydrochloric Acid