title: Nitric oxide potentiates acute lung injury in an isolated rabbit lung model.
abstract: BACKGROUND
  The effect of inhaled nitric oxide (NO) treatment on pulmonary function in the setting of adult respiratory distress syndrome is controversial. We examined the effect of inhaled NO on pulmonary function in an isolated rabbit lung model of oleic acid (OA)-induced acute lung injury. We hypothesized that NO would decrease pulmonary artery pressure and improve oxygenation.
  
  
  METHODS
  Rabbit heart-lung blocks were isolated, flushed in vivo, harvested, and immediately perfused with whole blood and ventilated with 50% oxygen (O2). Pulmonary artery pressure was determined every 15 seconds for 60 minutes of perfusion. Oxygenation was determined by blood gas analysis of pulmonary venous effluent at 0, 20, 40, and 60 minutes after initiation of OA infusion. Rabbits were randomized into four study groups: saline control; OA control, which received a 20-minute infusion of 50% OA/ethanol solution; NO treatment (20 ppm NO inhaled before OA infusion); and NO control, which underwent NO (20 ppm) pretreatment, followed by saline infusion. Pulmonary artery pressure, oxygenation (arteriovenous O2 difference), compliance, and wet/dry lung weight were determined.
  
  
  RESULTS
  Pretreatment with NO caused significant increases in pulmonary artery pressure (NO treatment versus NO control and saline control; no significant difference between NO treatment group and OA control group), and did not improve oxygenation in our model.
  
  
  CONCLUSIONS
  Contrary to our hypothesis, pretreatment with NO potentiates acute lung injury in our isolated lung model. There was significant exacerbation of pulmonary hypertension and no improvement in oxygenation. Further investigation of the possible deleterious effects of NO in acute lung injury are needed, especially in the early acute phases of this process.
authors.affiliation: Department of Surgery, University of Virginia Health Sciences Center, Charlottesville 22906-0005, USA.
authors.forename: C S
authors.initials: CS
authors.lastname: Rayhrer
authors.forename: T D
authors.initials: TD
authors.lastname: Edmisten
authors.forename: G A
authors.initials: GA
authors.lastname: Cephas
authors.forename: C G
authors.initials: CG
authors.lastname: Tribble
authors.forename: I L
authors.initials: IL
authors.lastname: Kron
authors.forename: J S
authors.initials: JS
authors.lastname: Young
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D000431:Ethanol / Q000009:adverse effects; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000503:physiopathology; D008168:Lung / Q000187:drug effects* / Q000503:physiopathology; D008170:Lung Compliance / Q000187:drug effects; D009569:Nitric Oxide / Q000009:adverse effects*; D019301:Oleic Acid / Q000009:adverse effects; D009929:Organ Size; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects; D011651:Pulmonary Artery / Q000187:drug effects; D011654:Pulmonary Edema / Q000139:chemically induced / Q000503:physiopathology; D011667:Pulmonary Veins; D011817:Rabbits; D011897:Random Allocation; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000503:physiopathology*; D012965:Sodium Chloride; D012997:Solvents / Q000009:adverse effects; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D012997:Solvents; D019301:Oleic Acid; D009569:Nitric Oxide; D000431:Ethanol; D012965:Sodium Chloride; D010100:Oxygen