title: Proinflammatory and prothrombotic status in emphysematous rats exposed to intermittent hypoxia.
abstract: OBJECTIVE
  To develop an "overlap syndrome (OS)" rat model by intermittent hypoxia (IH) exposure on the base of pre-existing emphysema, and to explore whether "OS" exposure results in more severe systemic inflammation, and whether the inflammation changes levels of coagulant/anticoagulant factors and oxidative stress status.
  
  
  METHODS
  Sixty Wistar rats were put into 4 groups: Control group; IH group, IH exposure; Emphysema group, smoke exposure; Overlap group, smoke exposure and IH exposure. We obtained peripheral blood for apoptosis of CD3(+)CD4(+), CD3(+)CD8(+) T lymphocytes and neutrophils, and for endothelial progenitor cell (EPC) counts. Tumor necrosis factor (TNF)-α, interleukin (IL)-6 and coagulant/anticoagulant factors [antithrombin (AT), fibrinogen (FIB), Factor VIII (FVIII) and von Willebrand factor (vWF)] were evaluated. We also obtained tissue blocks of lung, liver, pancreas, and right carotid artery for pathologic scoring and measurements of liver oxidative stress [superoxide dismutase (SOD) activity, catalase (CAT) activity and malondialdehyde (MDA) concentration].
  
  
  RESULTS
  The levels of TNF-α and IL-6, CD3(+)CD4(+) T lymphocyte apoptosis, EPC counts, coagulant factors and MDA are the highest in Overlap group, the lowest in Control group, when the levels of neutrophil apoptosis, CD3(+)CD8(+) T lymphocyte apoptosis, AT, SOD and CAT are the lowest in Overlap group, the highest in Control group (all P values < 0.05).
  
  
  CONCLUSIONS
  In model animals, when IH is combined with emphysema, there will be a more severe or an "overlapped" systemic/multiple organic inflammation, oxidative stress and hyper-coagulability. And the pro-inflammatory and pro-thrombotic status resulted from "OS" exposure may elicit a robust EPC mobilization, which needs further investigation.
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital Tianjin 300052, China.
authors.forename: Caili
authors.initials: C
authors.lastname: Li
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital Tianjin 300052, China.
authors.forename: Xiaokun
authors.initials: X
authors.lastname: Yang
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital Tianjin 300052, China ; Neuropharmacology Section, Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park NC 27709, USA.
authors.forename: Jing
authors.initials: J
authors.lastname: Feng
authors.affiliation: Departmen of Geriatric, Tianjin Medical University General Hospital Tianjin 300052, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Lei
authors.affiliation: Infective Disease Institute, Second Affiliated Hospital of Tianjin Medical University Tianjin, 300211, China.
authors.forename: Yubao
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004646:Emphysema / Q000473:pathology* / Q000503:physiopathology; D000860:Hypoxia / Q000473:pathology* / Q000503:physiopathology; D007249:Inflammation / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013927:Thrombosis / Q000473:pathology* / Q000503:physiopathology
keywords: Overlap syndrome; coagulant factors; emphysema; inflammation; intermittent hypoxia