title: Leukocyte depletion of blood cardioplegia attenuates reperfusion injury.
abstract: BACKGROUND
  Leukocytes are associated with myocardial injury during reperfusion after ischemia. Short periods of leukocyte depletion during reperfusion result in persistent attenuation of postischemic myocardial dysfunction.
  
  
  METHODS
  Leukocyte depletion was examined in a canine model of regional myocardial ischemia and reperfusion. The extracorporeal circuit and cardioplegia circuits underwent leukocyte depletion by mechanical filtration. Animals were instrumented for baseline global function before 90-minute occlusion of the left anterior descending coronary artery. Global function during ischemia and at 5, 30, 60, and 90 minutes after a 60-minute cardioplegic arrest using continuous blood cardioplegia was assessed in leukocyte-depleted (n = 9) and control (n = 10) groups.
  
  
  RESULTS
  No significant difference between groups was seen for systemic leukocyte counts, global function, or water content. Endothelial function was significantly protected as assessed by response to both calcium ionophore (endothelial-dependent, receptor-independent relaxation: leukocyte-depleted, 72% +/- 19% of endothelin-induced constriction versus control, 46% +/- 14%; p < 0.05) and acetylcholine (endothelial-dependent, receptor-dependent relaxation: leukocyte-depleted, 83% +/- 11% versus control, 44% +/- 15%; p < 0.05).
  
  
  CONCLUSIONS
  Leukocyte-mediated endothelial reperfusion injury can be attenuated by leukocyte depletion during reperfusion.
authors.affiliation: Division of Cardiothoracic Surgery, Emory University School of Medicine, Carlyle Fraser Heart Center, Emory/Crawford Long Hospital, Atlanta, Georgia, USA.
authors.forename: F E
authors.initials: FE
authors.lastname: Schmidt
authors.forename: M J
authors.initials: MJ
authors.lastname: MacDonald
authors.forename: C O
authors.initials: CO
authors.lastname: Murphy
authors.forename: W M
authors.initials: WM
authors.lastname: Brown
authors.forename: J P
authors.initials: JP
authors.lastname: Gott
authors.forename: R A
authors.initials: RA
authors.lastname: Guyton
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002315:Cardiopulmonary Bypass; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D004285:Dogs; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006324:Heart Arrest, Induced; D066298:In Vitro Techniques; D007958:Leukocyte Count; D007962:Leukocytes / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control; D009599:Nitroprusside / Q000494:pharmacology; D013318:Stroke Volume; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D009599:Nitroprusside; D000109:Acetylcholine