title: Oxidative stress precedes peak systemic inflammatory response in pediatric patients undergoing cardiopulmonary bypass operation.
abstract: Oxidative stress seems to contribute to cardiopulmonary bypass (CPB)-related postoperative complications. Pediatric patients are particularly prone to these complications. With this in mind, we measured oxidative stress markers in blood plasma of 20 children undergoing elective heart surgery before, during, and up to 48 h after cessation of CPB, along with inflammatory parameters and full analysis of iron status. Ascorbate levels were decreased by approximately 50% (P < 0.001) at the time of aorta cross-clamp removal (or pump switch-off in 4 patients with partial CPB), and associated with corresponding increases in dehydroascorbate (P < 0.001, r = -0.80) and malondialdehyde (P < 0.01, r = -0.59). In contrast to the immediate oxidative response, peak levels of IL-6 and IL-8 were not observed until 3-12 h after CPB cessation. The early loss of ascorbate correlated with duration of CPB (P < 0.002, r = 0.72), plasma hemoglobin after cross-clamp removal (P < 0.001, r = 0.70), and IL-6 and IL-8 levels at 24 and 48 h after CPB (P < 0.01), but not with postoperative lactate levels, strongly suggesting that hemolysis, and not inflammation or ischemia, was the main cause of early oxidative stress. The correlation of ventilation time with early changes in ascorbate (P < 0.02, r = 0.55), plasma hemoglobin (P < 0.01, r = 0.60), and malondialdehyde (P < 0.02, r = 0.54) suggests that hemolysis-induced oxidative stress may be an underlying cause of CPB-associated pulmonary dysfunction. Optimization of surgical procedures or therapeutic intervention that minimize hemolysis (e.g., off-pump surgery) or the resultant oxidative stress (e.g., antioxidant treatment) should be considered as possible strategies to lower the rate of postoperative complications in pediatric CPB.
authors.affiliation: Institute for Infectious Diseases, University of Berne, Friedbuehlstrasse 51, CH-3010 Berne, Switzerland. stephan.christen@ifik.unibe.ch
authors.forename: Stephan
authors.initials: S
authors.lastname: Christen
authors.forename: Barbara
authors.initials: B
authors.lastname: Finckh
authors.forename: Jens
authors.initials: J
authors.lastname: Lykkesfeldt
authors.forename: Peter
authors.initials: P
authors.lastname: Gessler
authors.forename: Manuela
authors.initials: M
authors.lastname: Frese-Schaper
authors.forename: Peter
authors.initials: P
authors.lastname: Nielsen
authors.forename: Edith R
authors.initials: ER
authors.lastname: Schmid
authors.forename: Bernhard
authors.initials: B
authors.lastname: Schmitt
mesh_terms: D001205:Ascorbic Acid / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D006348:Cardiac Surgical Procedures; D002315:Cardiopulmonary Bypass; D002648:Child; D002675:Child, Preschool; D003683:Dehydroascorbic Acid / Q000378:metabolism; D006330:Heart Defects, Congenital / Q000601:surgery*; D006461:Hemolysis / Q000276:immunology; D006801:Humans; D007223:Infant; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D007501:Iron / Q000378:metabolism; D007511:Ischemia; D008315:Malondialdehyde / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D018384:Oxidative Stress / Q000276:immunology*; D011014:Pneumonia / Q000276:immunology* / Q000473:pathology; D011183:Postoperative Complications / Q000209:etiology*; D011446:Prospective Studies
chemical_list: D015850:Interleukin-6; D016209:Interleukin-8; D008315:Malondialdehyde; D002097:C-Reactive Protein; D007501:Iron; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid