title: Continuous hemodiafiltration therapy ameliorates LPS-induced systemic inflammation in a rat model.
abstract: BACKGROUND
  Systemic inflammation can result in multiple organ dysfunction syndrome, a potentially life-threatening condition. Some reports suggest that continuous hemodiafiltration can effectively remove proinflammatory cytokines from circulation during systemic inflammation. In the present study, we investigated whether continuous hemodiafiltration therapy could prevent LPS-induced systemic inflammation and improve survival in a rat model.
  
  
  METHODS
  Male Wistar rats were injected with lipopolysaccharide (LPS; 7.5 mg/kg body weight), and 6 h later were treated with either single-pass hemofiltration (C group), continuous hemofiltration (CHF group), continuous hemodiafiltration (CHDF group), or mock filtration (Control group). We performed histologic examinations of lung and liver tissues, determined serum cytokine levels, and survival rates for each treatment group, and compared cytokine removal between CHF and CHDF therapies.
  
  
  RESULTS
  Histologic examination revealed significant reduction in inflammation in lung and liver tissues harvested 24 h after CHDF compared with the Control group. Likewise, LPS-induced serum TNF-α and IL-6 levels decreased with continuous hemodiafiltration along with a significant improvement in survival. After 30 min of treatment, both CHF and CHDF removed significant amounts of TNF-α and IL-6 from the blood. However, serum cytokine levels measured before and after filtration were not significantly different.
  
  
  CONCLUSIONS
  Continuous hemodiafiltration therapy lowered inflammatory cytokines and increased survival rates in a rat model of systemic inflammation. Therefore, continuous hemodiafiltration may be a potential therapy for use against various systemic inflammatory diseases.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, Yufu City, Oita, Japan. saku@med.oita-u.ac.jp
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hagiwara
authors.forename: Hideo
authors.initials: H
authors.lastname: Iwasaka
authors.forename: Akira
authors.initials: A
authors.lastname: Hasegawa
authors.forename: Seigo
authors.initials: S
authors.lastname: Hidaka
authors.forename: Aya
authors.initials: A
authors.lastname: Uno
authors.forename: Ueo
authors.initials: U
authors.lastname: Kaori
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Uchida
authors.forename: Takayuki
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D055371:Acute Lung Injury / Q000276:immunology / Q000517:prevention & control; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000276:immunology / Q000517:prevention & control; D004195:Disease Models, Animal; D024243:HMGB1 Protein / Q000097:blood; D017583:Hemodiafiltration / Q000379:methods*; D007249:Inflammation / Q000276:immunology / Q000628:therapy*; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015996:Survival Rate; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D024243:HMGB1 Protein; C104200:Hbp1 protein, rat; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha