title: Do vitamins C and E attenuate the effects of reactive oxygen species during pulmonary reperfusion and thereby prevent injury?
abstract: BACKGROUND
  We established an in vivo pig model of standardized lung ischemia to analyze pulmonary reperfusion injury. Enhanced chemiluminescence measurement (CM) allowed immediate quantification of reactive oxygen species (ROS) and subsequent lipid peroxidation. In such model we analyzed efficacy of vitamins C and E to prevent reperfusion injury.
  
  
  METHODS
  After left lateral thoracotomy in group I (n = 6), normothermic lung ischemia was maintained for 90 minutes followed by a 5-hour reperfusion period. In group II, animals (n = 6) underwent ischemia as in group I, but received vitamins (preoperative IV bolus C = 1 g, E = 0.75 g, then continuous infusion (125 mg/h) each throughout the study). In Group III, animals (n = 6) underwent sham surgery and served as controls. Hemodynamic variables and gas exchange were assessed. The CM was performed for injury quantification in blood samples and to determine activation of isolated PMNs. The Wilcox rank test was used for statistical analysis.
  
  
  RESULTS
  During reperfusion, all animals in group I developed significant pulmonary edema with significant loss of pulmonary function. The addition of vitamins (group II) improved oxygenation and almost abolished pulmonary inflammatory cell infiltration; however, as in group I, pulmonary compliance still tended to decline and the number of circulating leucocytes increased. The CM showed that, compared with group I, vitamins reduced O2- basic release by PMNs significantly (460% to 170%, p < 0.05; control 165%), but could not prevent an increase of free ROS in whole blood similar to group I (443% to 270%, p = ns, control 207%). With regard to lipid peroxidation only a trend of reduction was observed (117% to 105%, p = ns, control 100%).
  
  
  CONCLUSIONS
  Differentiated analysis by CM demonstrated that vitamins C and E inhibited PMN activation but were not able to prevent radical production by other sources. This offers a potential explanation why radical scavengers like vitamins only attenuate but ultimately do not prevent reperfusion injury.
authors.affiliation: Department of Cardiovascular Surgery, University Hospital Eppendorf, Hamburg, Germany. fl.wagner@uke.uni-hamburg.de
authors.forename: Florian M
authors.initials: FM
authors.lastname: Wagner
authors.forename: Andreas T
authors.initials: AT
authors.lastname: Weber
authors.forename: Katrin
authors.initials: K
authors.lastname: Ploetze
authors.forename: Felix
authors.initials: F
authors.lastname: Schubert
authors.forename: Steffen
authors.initials: S
authors.lastname: Pfeiffer
authors.forename: Steffen
authors.initials: S
authors.lastname: Albrecht
authors.forename: Stephan
authors.initials: S
authors.lastname: Schueler
mesh_terms: D000210:Acute-Phase Reaction / Q000503:physiopathology / Q000517:prevention & control; D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008168:Lung / Q000098:blood supply*; D008170:Lung Compliance / Q000187:drug effects / Q000502:physiology; D010100:Oxygen / Q000097:blood; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D013552:Swine; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D017382:Reactive Oxygen Species; D014810:Vitamin E; D001205:Ascorbic Acid; D010100:Oxygen