title: Hydroxyethyl starch 130/0.4 prevents the early pulmonary inflammatory response and oxidative stress after hemorrhagic shock and resuscitation in rats.
abstract: BACKGROUND
  This study was designed to determine the effects of various resuscitation fluids on pulmonary capillary leakage and pulmonary edema after HS and fluid resuscitation (HS/R) and to determine whether an antiinflammatory or antioxidative mechanism was involved.
  
  
  METHODS
  We induced HS by bleeding male Sprague-Dawley rats to a blood pressure of 30 to 40 mm Hg for 60 min. 60 min later, the rats were killed (HS group) or immediately resuscitated with L-isomer lactated Ringer's solution (HS+LR group), shed blood (HS+BL group), or hydroxyethyl starch (HS+HES group) to maintain the blood pressure to the original value during the 60-min resuscitation period. 3 h after resuscitation, pulmonary capillary leakage and wet/dry weight ratio, levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, malondialdehyde (MDA), oxidized and reduced glutathione (GSH and GSSG), myeloperoxidase (MPO) activity, nuclear factor (NF)-kappaB, activator protein (AP)-1 activation, and lung microscopic and ultrastructural histological changes were measured.
  
  
  RESULTS
  HES and BL treatment significantly improved pulmonary capillary leakage, wet/dry weight ratio and lung injuries after HS/R. In addition, both HES and BL could attenuate the increase in TNF-alpha, IL-6, MPO levels and NF-kappaB activation. However, HES but not BL could attenuate the increase in MDA level and GSSH/GSH ratio and AP-1 activation.
  
  
  CONCLUSIONS
  HES might attenuate pulmonary injuries by modulating pulmonary inflammatory response and oxidative stress, whereas BL attenuates pulmonary injuries by modulating pulmonary inflammatory response but not oxidative stress.
authors.affiliation: Research Institute of General Surgery, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
authors.forename: Pengfei
authors.initials: P
authors.lastname: Wang
authors.forename: Yousheng
authors.initials: Y
authors.lastname: Li
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002199:Capillary Permeability / Q000187:drug effects; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D006895:Hydroxyethyl Starch Derivatives / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D010952:Plasma Substitutes / Q000494:pharmacology; D011014:Pneumonia / Q000209:etiology / Q000517:prevention & control*; D011652:Pulmonary Circulation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation; D012771:Shock, Hemorrhagic / Q000150:complications*; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D006895:Hydroxyethyl Starch Derivatives; D015850:Interleukin-6; D016328:NF-kappa B; D010952:Plasma Substitutes; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D009195:Peroxidase; D005978:Glutathione; D019803:Glutathione Disulfide