title: Attenuation of sepsis-related immunoparalysis by continuous veno-venous hemofiltration in experimental porcine pancreatitis.
abstract: OBJECTIVE
  In light of evidence suggesting that hemofiltration favorably influences septic diseases by removing sepsis mediators, the impact of different modalities of continuous veno-venous hemofiltration (CVVH) on outcome and immunologic derangements in porcine pancreatogenic sepsis was evaluated.
  
  
  METHODS
  Randomized, controlled intervention trial.
  
  
  METHODS
  Forty-eight minipigs of either sex.
  
  
  METHODS
  Pancreatitis was induced by intraductal injection of sodium taurocholate (4%, 1 mL/kg body weight [BW]) and enterokinase (2 U/kg BW). Animals were allocated either to untreated controls-group 1-or to one of three treatment groups-group 2: low-volume CVVH (20 mL/kg BW), no change of hemofilters; group 3: low-volume CVVH, filters changed every 12 hrs; and group 4: high-volume CVVH (100 mL/kg BW), filters changed every 12 hrs. Survival represented the major parameter of the study. Serum cytokine levels, sepsis-related down-regulation of major histocompatibility complex II and CD14 expression on leukocytes, bacterial translocation, and endotoxemia were further parameters evaluated in the study.
  
  
  RESULTS
  High-volume CVVH combined with periodic filter change was significantly superior compared with less intensive treatment modalities (low-volume CVVH, no filter change) in sepsis protection. Long-term survival (>60 hrs) was found in 67% of group 4 and 33% of group 3 animals (p <.05), whereas in controls and group 2 no animal survived. CVVH ameliorated the initial serum tumor necrosis factor-alpha response and prevented sepsis-induced in vitro endotoxin hyporesponsiveness. Down-regulation of major histocompatibility complex II and CD14 expression on monocytes was significantly improved by CVVH. Improved oxidative burst and phagocytosis capacity in polymorphonuclear leukocytes suggested that leukocyte function was stabilized by CVVH. Also, CVVH significantly reduced bacterial translocation and endotoxemia.
  
  
  CONCLUSIONS
  Hemofiltration reversed sepsis-induced immunoparalysis in a porcine model of bile acid-induced pancreatitis. Implications for human pancreatitis must be validated in prospective, clinical protocols.
authors.affiliation: Department of Surgery, University Hospital Eppendorf, Hamburg, Germany.
authors.forename: E F
authors.initials: EF
authors.lastname: Yekebas
authors.forename: C F
authors.initials: CF
authors.lastname: Eisenberger
authors.forename: H
authors.initials: H
authors.lastname: Ohnesorge
authors.forename: A
authors.initials: A
authors.lastname: Saalmüller
authors.forename: H A
authors.initials: HA
authors.lastname: Elsner
authors.forename: M
authors.initials: M
authors.lastname: Engelhardt
authors.forename: A
authors.initials: A
authors.lastname: Gillesen
authors.forename: J
authors.initials: J
authors.lastname: Meins
authors.forename: M
authors.initials: M
authors.lastname: The
authors.forename: T
authors.initials: T
authors.lastname: Strate
authors.forename: C
authors.initials: C
authors.lastname: Busch
authors.forename: W T
authors.initials: WT
authors.lastname: Knoefel
authors.forename: C
authors.initials: C
authors.lastname: Bloechle
authors.forename: J R
authors.initials: JR
authors.lastname: Izbicki
mesh_terms: D000208:Acute Disease; D000818:Animals; D018988:Bacterial Translocation; D016207:Cytokines / Q000097:blood; D015536:Down-Regulation; D004731:Endotoxins / Q000097:blood; D005802:Genes, MHC Class II / Q000276:immunology; D006440:Hemofiltration; D007154:Immune System Diseases / Q000209:etiology / Q000276:immunology / Q000517:prevention & control*; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D009000:Monocytes / Q000276:immunology; D009102:Multiple Organ Failure / Q000209:etiology / Q000276:immunology / Q000517:prevention & control*; D009504:Neutrophils / Q000276:immunology; D010195:Pancreatitis / Q000276:immunology / Q000628:therapy*; D016019:Survival Analysis; D013552:Swine; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D004731:Endotoxins; D018950:Lipopolysaccharide Receptors; D014409:Tumor Necrosis Factor-alpha