title: Inflammatory response during simulated extracorporeal circulation with addition of nitric oxide.
abstract: BACKGROUND
  Heart operations performed with extracorporeal circulation (ECC) are associated with an inflammatory response. This response is partially due to granulocyte activation. Leukocyte derived free radicals are involved in tissue injury. The purpose of this study was to observe whether nitric oxide influence the inflammatory response during simulated ECC.
  
  
  METHODS
  In a model of simulated extracorporeal circulation, fresh whole human blood mixed with Ringer's solution was circulated through a heart-lung machine for three hours. In five circuits NO was added to oxygen/air mixture (group N), while five other circuits were ventilated with oxygen/air mixture (group C). The methods for estimating the inflammatory response were determination of oxygen free radicals production capacity, using chemiluminescence, and measurements of concentration of granulocyte derived proteins (myeloperoxidase and human neutrophil lipocalin).
  
  
  RESULTS
  All measured parameters were similarly independent of additional supply of nitric oxide almost throughout extracorporeal circulation time. The sole significant difference between the two groups was found at an early stage of extracorporeal circulation, when luminol-enhanced chemiluminescence in whole blood was higher in the N group (1,500, 1,470-1,950 vs 1,038, 750-1,050 in the control group; medians with quartiles). A similar tendency was observed in lucigenin-enhanced chemiluminescence at 60 min of extracorporeal circulation (625, 560-875 in the N group vs 400, 360-525 in the control group; medians with quartiles).
  
  
  CONCLUSIONS
  Nitric oxide supply does not influence inflammatory response during three hours long extracorporeal circulation, although some protective effect on hydrogen peroxide production in whole blood was detected in the initial phase of extracorporeal circulation.
authors.affiliation: Department of Cardiothoracic Surgery, Uppsala University Hospital, Sweden.
authors.forename: J W
authors.initials: JW
authors.lastname: Borowiec
authors.forename: M
authors.initials: M
authors.lastname: Lahtinen
authors.forename: P
authors.initials: P
authors.lastname: Venge
authors.forename: A
authors.initials: A
authors.lastname: Henze
authors.forename: H
authors.initials: H
authors.lastname: Stiernström
mesh_terms: D000166:Acridines; D000209:Acute-Phase Proteins; D015415:Biomarkers / Q000097:blood; D002352:Carrier Proteins / Q000097:blood; D005112:Extracorporeal Circulation / Q000009:adverse effects*; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D007202:Indicators and Reagents; D007958:Leukocyte Count; D000071068:Lipocalin-2; D054834:Lipocalins; D008163:Luminescent Measurements; D008165:Luminol; D008955:Models, Cardiovascular; D009504:Neutrophils / Q000378:metabolism; D009569:Nitric Oxide / Q000627:therapeutic use*; D015513:Oncogene Proteins; D009195:Peroxidase / Q000097:blood; D011518:Proto-Oncogene Proteins; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology* / Q000517:prevention & control
chemical_list: D000166:Acridines; D000209:Acute-Phase Proteins; D015415:Biomarkers; D002352:Carrier Proteins; D016166:Free Radical Scavengers; D006454:Hemoglobins; D007202:Indicators and Reagents; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; C033472:10,10'-dimethyl-9,9'-biacridinium; D009569:Nitric Oxide; D008165:Luminol; D009195:Peroxidase