title: Reduced expression of systemic proinflammatory cytokines after off-pump versus conventional coronary artery bypass grafting.
abstract: BACKGROUND
  Both cardiopulmonary bypass (CPB) and operative trauma are associated with increased expression of proinflammatory cytokines. We assessed the relative contribution of CPB on activation of various proinflammatory cytokines in patients undergoing coronary revascularization by comparing them with patients receiving coronary artery bypass grafts using off-pump (OPCAB) techniques.
  
  
  METHODS
  Twenty-six patients were assigned to either the OPCAB procedure using a suction device and regular sternotomy (n = 13) or were treated conventionally using extracorporeal circulation, blood cardioplegia and hypothermic arrest (29-31 degrees C; n = 13). C-reactive protein and systemic levels of TNF-alpha, TNF specific receptors Rp1 and Rp2, Interleukin-6 (IL-6) and soluble IL-2 receptors (sIL-2r) were assayed by ELISA or EIA. To account for systemic nitric oxide production, total nitrate/nitrite (NOx) was measured using the Griess reaction.
  
  
  RESULTS
  Coronary revascularization with CPB was associated with a significant expression increase in the TNF-system and sIL-2r when compared to the OPCAB patients. Although IL-6 expression did not differ between both groups, C-reactive protein levels were significantly lower in the OPCAB group. Moreover, systemic NOx levels as the stable end-product of nitric oxide were lower in the OPCAB group.
  
  
  CONCLUSIONS
  The data of the present study indicate that, despite comparable surgical trauma, the OPCAB revascularization procedure without the use of CPB and cardioplegic arrest significantly reduces the systemic inflammatory response syndrome and early catecholamine requirement. This may contribute to improved organ function, subsequently resulting in improved postoperative recovery from surgical revascularization procedures, particularly in critically ill patients.
authors.affiliation: Department of Cardiac Surgery, Ludwig-Maximilians University, Munich, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Schulze
authors.forename: N
authors.initials: N
authors.lastname: Conrad
authors.forename: A
authors.initials: A
authors.lastname: Schütz
authors.forename: K
authors.initials: K
authors.lastname: Egi
authors.forename: H
authors.initials: H
authors.lastname: Reichenspurner
authors.forename: B
authors.initials: B
authors.lastname: Reichart
authors.forename: S M
authors.initials: SM
authors.lastname: Wildhirt
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000097:blood / Q000378:metabolism; D002097:C-Reactive Protein / Q000032:analysis; D001026:Coronary Artery Bypass / Q000379:methods*; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D011184:Postoperative Period; D015375:Receptors, Interleukin-2 / Q000097:blood; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood / Q000378:metabolism; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015703:Antigens, CD; D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D009566:Nitrates; D009573:Nitrites; D015375:Receptors, Interleukin-2; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein