title: Attenuation of changes in leukocyte surface markers and complement activation with heparin-coated cardiopulmonary bypass.
abstract: BACKGROUND
  The inflammatory response induced by cardiopulmonary bypass can result in severe organ dysfunction in some patients. This postperfusion response is caused mainly by contact between blood and the foreign surface of the cardiopulmonary bypass equipment and includes adhesion of leukocytes to vascular endothelium, which precedes a series of events that mediate inflammatory damage to tissues.
  
  
  METHODS
  Low-risk patients accepted for coronary artery bypass grafting were randomized to operation with the cardiopulmonary bypass surface either completely heparin coated (Duraflo II) or uncoated. There were 12 patients in each group. Blood plasma sampled during cardiopulmonary bypass was analyzed for complement activation (C3bc and terminal SC5b-9 complement complex) and neutrophil activation (lactoferrin and myeloperoxidase). In addition, neutrophils, monocytes, and platelets were counted, and the expression of surface markers on the neutrophils and monocytes (complement receptor [CR] 1, CR3, CR4, and L-selectin) and on the platelets (P-selectin and CD41) was quantified with flow cytometry.
  
  
  RESULTS
  Clinical and surgical results were similar in both groups. In the group with the heparin-coated surface, the formation of the terminal SC5b-9 complement complex was significantly reduced, and the counts of circulating leukocytes and platelets were significantly less reduced initially but were higher at the end of cardiopulmonary bypass compared with baseline. Also, the expression of CR1, CR3, and CR4 was significantly less upregulated and the L-selectin, significantly less downregulated on monocytes and neutrophils.
  
  
  CONCLUSIONS
  We conclude that heparin coating reduces complement activation and attenuates the leukocyte integrin and selectin response that occurs when uncoated circuits are used.
authors.affiliation: Department of Cardiothoracic Surgery, Ullevål Hospital, University of Oslo, Norway.
authors.forename: O
authors.initials: O
authors.lastname: Moen
authors.forename: K
authors.initials: K
authors.lastname: Høgåsen
authors.forename: E
authors.initials: E
authors.lastname: Fosse
authors.forename: E
authors.initials: E
authors.lastname: Dregelid
authors.forename: V
authors.initials: V
authors.lastname: Brockmeier
authors.forename: P
authors.initials: P
authors.lastname: Venge
authors.forename: M
authors.initials: M
authors.lastname: Harboe
authors.forename: T E
authors.initials: TE
authors.lastname: Mollnes
mesh_terms: D000954:Antigens, Surface / Q000378:metabolism*; D001672:Biocompatible Materials; D002315:Cardiopulmonary Bypass / Q000009:adverse effects / Q000295:instrumentation*; D003167:Complement Activation; D001026:Coronary Artery Bypass; D005260:Female; D006493:Heparin; D006801:Humans; D007958:Leukocyte Count; D008213:Lymphocyte Activation; D008297:Male; D010976:Platelet Count
chemical_list: D000954:Antigens, Surface; D001672:Biocompatible Materials; D006493:Heparin