title: Protective effects of hydroxyethyl starch 130/0.4 against myocardial ischemia/reperfusion injury in rats.
abstract: BACKGROUND
  The effects of hydroxyethyl starch 130/0.4 (HES130/0.4) on myocardial ischemia/reperfusion (I/R) injury and its mechanism are uncertain. The aim of this study was to investigate the protective effects of HES 130/0.4 on myocardial I/R injury.
  
  
  METHODS
  Forty-eight Sprague-Dawley rats were assigned to sham-operation group (S group), ischemia-reperfusion group (I/R group), albumin-I/R group (A-I/R group) and HES130/0.4-I/R group (H-I/R group). The fluids were administered at 25 minutes after ischemia. H-I/R group was given 7.5 ml/kg of HES 130/0.4; I/R group and A-I/R group received the same volume of normal saline and 5% albumin, respectively. The rats in S group were sham operated and received the same fluid as I/R group. After 30 minutes of ischemia and 3 hours of reperfusion, blood samples were taken for cytokines assay, myocardium was excised for detection of NF-κB activity and myocardial infarction areas were taken for immunohistochemical analysis.
  
  
  RESULTS
  Hemodynamic parameters of H-I/R group were better than I/R and A-I/R groups at all designated time points. The results of 2,3,5-triphenyl-tetrazolium (TTC) and HE staining were better in the H-I/R group. Myeloperoxidase (MPO), NF-κB activity and concentrations of TNF-α, IL-1β were elevated markedly in I/R groups. HES130/0.4 lessened the release of TNF-α and IL-1β consistent with the reduction of MPO activity, and HES 130/0.4 inhibited the activity of NF-κB in H-I/R group. The number of apoptotic cells in the H-I/R group was also significantly reduced compared with I/R and A-I/R group
  
  
  CONCLUSIONS
  HES130/0.4 has a protective effect on I/R injured myocardium, probably by inhibiting NF-κB activity, reducing the release of pro-inflammatory cytokines and interfering with the apoptosis of cardiomyocytes.
authors.affiliation: Department of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
authors.forename: Hai-Jing
authors.initials: HJ
authors.lastname: Sun
authors.forename: Hao
authors.initials: H
authors.lastname: Li
authors.forename: Zui
authors.initials: Z
authors.lastname: Zou
authors.forename: Xue-Yin
authors.initials: XY
authors.lastname: Shi
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000187:drug effects; D006895:Hydroxyethyl Starch Derivatives / Q000627:therapeutic use*; D053583:Interleukin-1beta / Q000378:metabolism; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C485123:HES 130-0.4; D006895:Hydroxyethyl Starch Derivatives; D053583:Interleukin-1beta; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase