title: Effects of long-term hemofiltration on circulating mediators and superoxide production during continuous endotoxin administration.
abstract: BACKGROUND
  The purpose of this study was to test whether continuous hemofiltration eliminates cytokines and eicosanoids, or stimulates granulocyte function.
  
  
  METHODS
  Nineteen pigs were divided into a control group (n = 7), a hemofiltration group (n = 7), and an extracorporeal circuit only group (n = 5). All animals received the same amount of intravenous endotoxin and resuscitation fluid. Zero-balanced hemofiltration was started 30 minutes after initiation of endotoxemia and continued throughout the experiment. Plasma endotoxin, tumor necrosis factor-alpha, eicosanoids, superoxide production, and other physiologic parameters were measured before challenge and at scheduled intervals thereafter.
  
  
  RESULTS
  Eicosanoids were filtered but plasma concentrations were not reduced. Tumor necrosis factor-alpha was not filtered or adsorbed. There were no significant differences between groups in any measured parameters.
  
  
  CONCLUSIONS
  Continuous hemofiltration could not efficiently remove tumor necrosis factor-alpha or eicosanoids. Also, continuous hemofiltration did not stimulate production of the proinflammatory mediators measured, nor improve respiratory distress.
authors.affiliation: U.S. Army Institute of Surgical Research, Fort Sam Houston, Texas 78234-5012, USA.
authors.forename: S
authors.initials: S
authors.lastname: Ishihara
authors.forename: J A
authors.initials: JA
authors.lastname: Ward
authors.forename: O
authors.initials: O
authors.lastname: Tasaki
authors.forename: W W
authors.initials: WW
authors.lastname: Brinkley
authors.forename: L G
authors.initials: LG
authors.lastname: Seraile
authors.forename: B A
authors.initials: BA
authors.lastname: Pruitt
authors.forename: D W
authors.initials: DW
authors.lastname: Mozingo
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D004731:Endotoxins / Q000008:administration & dosage*; D004926:Escherichia coli; D005260:Female; D006098:Granulocytes / Q000378:metabolism; D006440:Hemofiltration; D006861:Hydrogen Peroxide / Q000378:metabolism; D018836:Inflammation Mediators / Q000097:blood*; D007262:Infusions, Intravenous; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008168:Lung / Q000473:pathology; D015656:Respiratory Mechanics; D018805:Sepsis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D013481:Superoxides / Q000378:metabolism*; D013552:Swine; D013929:Thromboxane B2 / Q000097:blood; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D004731:Endotoxins; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C044101:endotoxin, Escherichia coli; D006861:Hydrogen Peroxide