title: Controlled reoxygenation during cardiopulmonary bypass decreases markers of organ damage, inflammation, and oxidative stress in single-ventricle patients undergoing pediatric heart surgery.
abstract: OBJECTIVE
  Single-ventricle patients undergoing pediatric heart surgery are a high-risk group owing to reoxygenation injury during cardiopulmonary bypass (CPB). The present study investigated the effects of controlled reoxygenation CPB on biomarkers of organ damage, inflammation, stress, and long-term functional outcomes in cyanotic patients with either a single or double ventricle during open heart surgery.
  
  
  METHODS
  Cyanotic patients with either a single (n = 32) or double (n = 47) ventricle undergoing surgical correction were randomized to receive CPB using either standard oxygen levels or controlled reoxygenation. The markers of cardiac injury, inflammation, stress, and cerebral and hepatic injury were measured preoperatively, at 10 and 30 minutes after starting CPB, and at 10 minutes and 4 and 24 hours after CPB. The data were analyzed using a mixed regression model.
  
  
  RESULTS
  No difference was found in the pre- or intraoperative characteristics between the standard and controlled reoxygenation CPB groups for single- or double-ventricle patients. In the single-ventricle patients, controlled reoxygenation CPB significantly (P < .05) decreased the markers of organ damage, inflammation, stress, and oxidative stress. In contrast, the markers of inflammation and cardiac injury were not altered by controlled reoxygenation CPB in the double-ventricle patients.
  
  
  CONCLUSIONS
  Controlled reoxygenation CPB decreased the markers of organ damage, stress, inflammation, and oxidative stress in single-ventricle patients undergoing cardiac surgery.
authors: Bristol Royal Hospital for Children, Bristol, United Kingdom; Rush University Medical Center, Chicago, Ill. Electronic address: M.Caputo@bristol.ac.uk.
authors: Massimo
authors: M
authors: Caputo
authors: Bristol Heart Institute, University of Bristol, Bristol, United Kingdom.
authors: Amir
authors: A
authors: Mokhtari
authors: Bristol Heart Institute, University of Bristol, Bristol, United Kingdom.
authors: Antonio
authors: A
authors: Miceli
authors: Bristol Heart Institute, University of Bristol, Bristol, United Kingdom.
authors: Mohamed T
authors: MT
authors: Ghorbel
authors: Bristol Heart Institute, University of Bristol, Bristol, United Kingdom.
authors: Gianni D
authors: GD
authors: Angelini
authors: Rush University Medical Center, Chicago, Ill.
authors: Andrew J
authors: AJ
authors: Parry
authors: Bristol Heart Institute, University of Bristol, Bristol, United Kingdom.
authors: Saadeh M
authors: SM
authors: Suleiman
mesh_terms: D000367:Age Factors; D015415:Biomarkers / Q000097:blood; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D002648:Child; D002675:Child, Preschool; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004739:England; D005260:Female; D006330:Heart Defects, Congenital / Q000097:blood / Q000601:surgery*; D006352:Heart Ventricles / Q000002:abnormalities / Q000378:metabolism / Q000601:surgery*; D006801:Humans; D007223:Infant; D007249:Inflammation / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D018384:Oxidative Stress; D010102:Oxygen Inhalation Therapy / Q000009:adverse effects / Q000379:methods*; D010313:Partial Pressure; D013997:Time Factors; D016896:Treatment Outcome; D014336:Troponin / Q000097:blood
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D014336:Troponin; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost