title: [Establishment of delayed encephalopathy rat model of carbon monoxide poisoning].
abstract: OBJECTIVE
  To establish the delayed encephalopathy rat model of carbon monoxide (CO) poisoning.
  
  
  METHODS
  40 Wistar rats were randomly divided into 4 groups of 10 rats and were placed in the chambers of inside-built 10-chamber poisoning box. Mixed gas is ventilated with the volume fractions of 10.0 x 10(-4), 15.0 x 10(-4) and 16.5 x 10(-4) of CO in air into the chambers for group A, B and C respectively, and pure air was ventilated for group D. The gas flow rate was 800 L/h in the first 5 hours, 1,000 L/h in the middle 4 hours, and 1,200 L/h in the last 3 hours, with a whole ventilation time of 12 hours. Before and after CO poisoning maze test with radial eight-arm maze was conducted to assess the rats' intelligence. The appearance of coma or less than 3 correct arm-enterings in maze test between the 3rd and 28th day after poisoning was considered as the indications of delayed encephalopathy. TUNEL method, flow cytometry, and transmission electron microscopy were adopted to examine the cellular apoptosis in cerebral cortex and hippocampus area.
  
  
  RESULTS
  There were 4 rats with delayed encephalopathy changes in groups B and C respectively, while no similar behavioral change appeared in groups A and D. TUNEL method showed an apoptotic rate of 45.0% to 65.0% in the rats with delayed encephalopathy of group B and an apoptotic rate of 55.0% to 80.0% in the rats with delayed encephalopathy of group C, most of the apoptotic cells being neurons. Flow cytometry showed an apoptotic rate of 50.5% +/- 4.2% in the rats with delayed encephalopathy of group B and an apoptotic rate of 55.9% +/- 7.8% in the rats with delayed encephalopathy of group C. By electron microscopy the percentage of typical apoptotic neurons was 5.0% approximately 15% in group B and 10.0% to 20.0% in group C, less than 5.0% in group A, and less than 1.6% in group D.
  
  
  CONCLUSIONS
  A delayed encephalopathy rat model of CO poisoning has been successfully established based on the volume fraction of 15.0 x 10(-4) to 16.5 x 10(-4) of CO in air and a poisoning time of 12 hours. The pathological change is a mass neuron apoptosis in cerebral cortex and hippocampus.
authors.affiliation: Department of Neurology, No 159 Hospital of Chinese People's Liberation Army, Zhumadian, Henan Province, 463000, China.
authors.forename: Fengchao
authors.initials: F
authors.lastname: Liu
authors.forename: Shusu
authors.initials: S
authors.lastname: Guo
authors.forename: Baosheng
authors.initials: B
authors.lastname: Lü
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
authors.forename: Bingzhen
authors.initials: B
authors.lastname: Cao
authors.forename: Chunfu
authors.initials: C
authors.lastname: Chen
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
authors.forename: Xinli
authors.initials: X
authors.lastname: Li
authors.forename: Zhengxiang
authors.initials: Z
authors.lastname: Cheng
authors.forename: Jin
authors.initials: J
authors.lastname: Wen
mesh_terms: D000818:Animals; D002248:Carbon Monoxide / Q000633:toxicity*; D002249:Carbon Monoxide Poisoning / Q000097:blood* / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D020287:In Situ Nick-End Labeling; D018782:Maze Learning; D020258:Neurotoxicity Syndromes / Q000097:blood* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D002248:Carbon Monoxide