title: Influence of hydroxyethyl starch 130/0.4 in pulmonary neutrophil recruitment and acute lung injury during polymicrobial sepsis in rats.
abstract: BACKGROUND
  Acute lung injury (ALI) is a progressive syndrome associated with significant mortality in sepsis patients. Neutrophils are key cells in the inflammatory response that characterizes ALI. This study was designed to explore the effects of hydroxyethyl starch (HES) 130/0.4 (a novel plasma substitute) on pulmonary neutrophil recruitment and associated ALI in a rat sepsis model induced by cecal ligation and puncture (CLP).
  
  
  METHODS
  Animals were randomly assigned to six groups [saline control; CLP and saline; CLP and HES (7.5, 15 and 30 ml/kg); and HES control], subjected to CLP and infused with or without HES 130/0.4 4 h after CLP. Six hours later, the pulmonary capillary permeability (PCP), myeloperoxidase (MPO) activity, lung histological changes, tumor necrosis factor-alpha, interleukin-1beta and cytokine-induced neutrophil chemoattractant levels, P-selectin mRNA expression and nuclear factor-kappa B (NF-kappaB) activation were measured.
  
  
  RESULTS
  Resuscitation with HES 130/0.4 significantly attenuated the CLP-induced increase in PCP, MPO activity, cytokine/chemokine levels, mRNA expression of P-selectin and NF-kappaB activation, all of which are involved in the recruitment of neutrophils. Groups receiving the higher doses of HES 130/0.4 (15 and 30 ml/kg) were more adequately resuscitated.
  
  
  CONCLUSIONS
  HES 130/0.4 can inhibit CLP-induced neutrophil recruitment and subsequent ALI by attenuating cytokines/chemokines, adhesion molecule-mediated inflammation and NF-kappaB activation.
authors.affiliation: Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
authors.forename: X
authors.initials: X
authors.lastname: Feng
authors.forename: B
authors.initials: B
authors.lastname: Ren
authors.forename: W
authors.initials: W
authors.lastname: Xie
authors.forename: Z
authors.initials: Z
authors.lastname: Huang
authors.forename: J
authors.initials: J
authors.lastname: Liu
authors.forename: R
authors.initials: R
authors.lastname: Guan
authors.forename: M
authors.initials: M
authors.lastname: Duan
authors.forename: J
authors.initials: J
authors.lastname: Xu
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology; D019743:Chemokines, CXC / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006339:Heart Rate / Q000187:drug effects; D006895:Hydroxyethyl Starch Derivatives / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008171:Lung Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects*; D019007:P-Selectin / Q000096:biosynthesis; D009195:Peroxidase / Q000378:metabolism; D010952:Plasma Substitutes / Q000494:pharmacology*; D011652:Pulmonary Circulation / Q000502:physiology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018805:Sepsis / Q000150:complications* / Q000378:metabolism / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D019743:Chemokines, CXC; D006895:Hydroxyethyl Starch Derivatives; D053583:Interleukin-1beta; D016328:NF-kappa B; D019007:P-Selectin; D010952:Plasma Substitutes; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase