title: Hydroxyethyl starch, but not modified fluid gelatin, affects inflammatory response in a rat model of polymicrobial sepsis with capillary leakage.
abstract: BACKGROUND
  Intravascular volume therapy is crucial in septic patients to improve tissue perfusion and maintain stable hemodynamics. Modified fluid gelatins (MFG) and medium weight hydroxyethyl starches (HES) are the most widely used synthetic colloids. Our aim in this study, performed in septic rats challenged by cecal ligation and puncture (CLP), was to investigate the effects of HES and MFG on pulmonary capillary leakage and to determine whether an antiinflammatory mechanism was involved.
  
  
  METHODS
  Animals were randomly allocated to eight groups: saline control; CLP and saline; CLP and HES (7.5, 15, and 30 mL/kg); CLP and MFG (7.5, 15, and 30 mL/kg). Each group had 20 rats, 10 of which were used for pulmonary capillary leakage and 10 for other measurements. Four hours after CLP, the specified doses of HES or MFG were infused. Six hours after surgery, pulmonary capillary leakage, levels of tumor necrosis factor-alpha, interleukin-1beta, and macrophage inflammatory protein-2, intercellular adhesion molecule-1 mRNA expression, myeloperoxidase activity, lung histological changes, and nuclear factor-kappaB activation were measured.
  
  
  RESULTS
  HES and MFG significantly attenuated the increase in capillary leakage in a dose-dependent manner. In addition, HES could decrease tumor necrosis factor-alpha, interleukin-1beta, and macrophage inflammatory protein-2 expression, intercellular adhesion molecule-1 mRNA expression, myeloperoxidase activity, neutrophil infiltration, and nuclear factor-kappaB activation, whereas MFG could not.
  
  
  CONCLUSIONS
  HES may attenuate capillary leakage by modulating an inflammatory response, whereas an antiinflammatory mechanism was not involved in the effects of MFG on capillary leakage.
authors.affiliation: Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, People's Republic of China.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Feng
authors.forename: Wei
authors.initials: W
authors.lastname: Yan
authors.forename: Zhaomin
authors.initials: Z
authors.lastname: Wang
authors.forename: Jian
authors.initials: J
authors.lastname: Liu
authors.forename: Min
authors.initials: M
authors.lastname: Yu
authors.forename: Sihai
authors.initials: S
authors.lastname: Zhu
authors.forename: Jianguo
authors.initials: J
authors.lastname: Xu
mesh_terms: D000818:Animals; D002196:Capillaries / Q000473:pathology*; D054426:Chemokine CXCL2; D019743:Chemokines, CXC / Q000096:biosynthesis; D005780:Gelatin / Q000494:pharmacology*; D006895:Hydroxyethyl Starch Derivatives / Q000494:pharmacology*; D007249:Inflammation / Q000188:drug therapy; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D053583:Interleukin-1beta / Q000378:metabolism; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D009195:Peroxidase / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000276:immunology* / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D054426:Chemokine CXCL2; D019743:Chemokines, CXC; C513296:Cxcl2 protein, rat; D006895:Hydroxyethyl Starch Derivatives; D053583:Interleukin-1beta; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D005780:Gelatin; D009195:Peroxidase