title: Modulation of the inflammatory response to cardiopulmonary bypass by dopexamine and epidural anesthesia.
abstract: BACKGROUND
  Cardiopulmonary bypass (CPB) induces a systemic inflammatory reaction. Microcirculation-dependent alteration of the gut mucosal barrier with subsequent translocation of endotoxins is a postulated mechanism for this inflammatory response. This study was designed to elucidate whether two different approaches to modulate splanchnic perfusion may influence systemic inflammation to CPB.
  
  
  METHODS
  We examined 40 patients scheduled for elective coronary bypass surgery in a prospective, randomized study. One group (DPX) received dopexamine (1 micro g. kg-1. min-1) continuously after induction of anesthesia until 18 h after CPB. The control group (CON) received equal volumes of NaCl 0.9% in a time-matched fashion. In a third group (EPI) a continuous epidural infusion of bupivacaine 0.25% [(body height (cm) - 100). 10-1=ml.h-1] was administered for the whole study period. Procalcitonin (PCT), tumor necrosis factor (TNF-alpha), soluble TNF receptor, human soluble intercellular adhesion molecule-1, C-reactive protein (CRP) and leukocyte count were measured as parameters of inflammation.
  
  
  RESULTS
  All parameters significantly increased following CPB. Increases of PCT, TNF-alpha and leukocyte count were significantly attenuated in the DPX and EPI groups at different time points. However, neither splanchnic blood flow nor oxygen delivery and consumption were different when compared with the CON-group.
  
  
  CONCLUSIONS
  These results do suggest that mechanisms other than an improved splanchnic blood flow by DPX and EPI treatment have to be considered for the anti-inflammatory effects.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, University of Saarland, Homburg/Saarland, Germany.
authors.forename: F
authors.initials: F
authors.lastname: Bach
authors.forename: U
authors.initials: U
authors.lastname: Grundmann
authors.forename: M
authors.initials: M
authors.lastname: Bauer
authors.forename: H
authors.initials: H
authors.lastname: Buchinger
authors.forename: S
authors.initials: S
authors.lastname: Soltész
authors.forename: T
authors.initials: T
authors.lastname: Graeter
authors.forename: R
authors.initials: R
authors.lastname: Larsen
authors.forename: M
authors.initials: M
authors.lastname: Silomon
mesh_terms: D000368:Aged; D000767:Anesthesia, Epidural; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002097:C-Reactive Protein / Q000187:drug effects; D002116:Calcitonin / Q000187:drug effects; D015740:Calcitonin Gene-Related Peptide; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D004298:Dopamine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood / Q000187:drug effects; D019344:Lactic Acid / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D011498:Protein Precursors / Q000187:drug effects; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; C000606589:CALCA protein, human; D011498:Protein Precursors; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D019344:Lactic Acid; C046318:dopexamine; D002116:Calcitonin; D002097:C-Reactive Protein; D015740:Calcitonin Gene-Related Peptide; D004298:Dopamine