title: Hypertonic saline solution reduces the inflammatory response in endotoxemic rats.
abstract: OBJECTIVE
  Volume replacement in septic patients improves hemodynamic stability. This effect can reduce the inflammatory response. The objective of this study was to evaluate the effect of 7.5% hypertonic saline solution versus 0.9% normal saline solution for volume replacement during an inflammatory response in endotoxemic rats.
  
  
  METHODS
  We measured cytokines (serum and gut), nitrite, and lipid peroxidation (TBARS) as indicators of oxidative stress in the gut. Rats were divided into four groups: control group (C) that did not receive lipopolysaccharide; lipopolysaccharide injection without treatment (LPS); lipopolysaccharide injection with saline treatment (LPS +S); and lipopolysaccharide injection with hypertonic saline treatment (LPS +H). Serum and intestine were collected. Measurements were taken at 1.5, 8, and 24 h after lipopolysaccharide administration.
  
  
  RESULTS
  Of the four groups, the LPS +H group had the highest survival rate. Hypertonic saline solution treatment led to lower levels of IL-6, IL-10, nitric oxide, and thiobarbituric acid reactive substances compared to 0.9% normal saline. In addition, hypertonic saline treatment resulted in a lower mortality compared to 0.9% normal saline treatment in endotoxemic rats. Volume replacement reduced levels of inflammatory mediators in the plasma and gut.
  
  
  CONCLUSIONS
  Hypertonic saline treatment reduced mortality and lowered levels of inflammatory mediators in endotoxemic rats. Hypertonic saline also has the advantage of requiring less volume replacement.
authors.affiliation: Faculdade de Medicina da Universidade de São Paulo, Emergency Medicine Division, São Paulo/SP, Brazil.
authors.forename: Mariana Cardillo
authors.initials: MC
authors.lastname: Theobaldo
authors.forename: Hermes Vieira
authors.initials: HV
authors.lastname: Barbeiro
authors.forename: Denise Frediani
authors.initials: DF
authors.lastname: Barbeiro
authors.forename: Ricardo
authors.initials: R
authors.lastname: Petroni
authors.forename: Francisco Garcia
authors.initials: FG
authors.lastname: Soriano
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D019446:Endotoxemia / Q000139:chemically induced / Q000378:metabolism*; D006439:Hemodynamics / Q000187:drug effects; D018836:Inflammation Mediators / Q000097:blood; D015212:Inflammatory Bowel Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D009573:Nitrites / Q000378:metabolism*; D018384:Oxidative Stress; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D016019:Survival Analysis; D018746:Systemic Inflammatory Response Syndrome / Q000378:metabolism / Q000628:therapy*
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D007378:Interleukins; D008070:Lipopolysaccharides; D009573:Nitrites; D012462:Saline Solution, Hypertonic; D016753:Interleukin-10