Effects of long-term hemofiltration on circulating mediators and superoxide production during continuous endotoxin administration

J Trauma. 1999 May;46(5):894-9. doi: 10.1097/00005373-199905000-00020.

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.

Conclusion: 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.

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / blood
  • Animals
  • Endotoxins / administration & dosage*
  • Escherichia coli
  • Female
  • Granulocytes / metabolism
  • Hemofiltration*
  • Hydrogen Peroxide / metabolism
  • Inflammation Mediators / blood*
  • Infusions, Intravenous
  • Lipopolysaccharides / administration & dosage
  • Lung / pathology
  • Respiratory Mechanics
  • Sepsis / metabolism*
  • Sepsis / pathology
  • Sepsis / physiopathology
  • Sepsis / therapy
  • Superoxides / metabolism*
  • Swine
  • Thromboxane B2 / blood
  • Time Factors
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • Endotoxins
  • Inflammation Mediators
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Superoxides
  • Thromboxane B2
  • 6-Ketoprostaglandin F1 alpha
  • endotoxin, Escherichia coli
  • Hydrogen Peroxide