title: Cholangiocytes of cirrhotic rats are more tolerant to ischemia than normal rats: a role for abnormal hepatic arteriovenous communications?
abstract: BACKGROUND
  To assess whether cholangiocytes of rats with liver cirrhosis are more tolerant to ischemic changes than normal rats, and whether this is due to arteriovenous fistulas.
  
  
  METHODS
  Ninety-eight Sprague-Dawley rats were divided into the normal group (n = 30) and the cirrhosis group (n = 68), and then each group was divided into controls and those with bile duct ischemia. At 0 h, 6 h, 3 d, and 14 d after the induction of bile duct ischemia, the liver of each rat was removed and stained with toluidine blue to compare cholangiocyte morphology. Cholangiocyte apoptosis was evaluated by a deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) assay. Expression of VEGF, HIF1, NF-kB(p65) was assessed by quantitative analysis of the products of reverse-transcriptase polymerase chain reaction. Resin casts were used to reproduce the intrahepatic vasculature of cirrhotic rats, and the presence of communications between the portal vein and hepatic artery was assessed with stereomicroscopy.
  
  
  RESULTS
  Rats with liver cirrhosis were more tolerant than normal rats 6 h after bile duct ischemia (P < 0.05); at 3 and 14 d after the ischemic insult, there was no significant difference between the cirrhotic rats and normal rats. Levels of expression of VEGF, HIF1, and NF-kB(p65) genes, either in normal rats or cirrhotic rats, were significantly elevated compared with those in the control group (∗, ∗∗P < 0.05), but a lower extent changes appeared in the cirrhotic rats (∗∗∗P < 0.05). Several communications could be observed between the portal vein and hepatic artery.
  
  
  CONCLUSIONS
  Cholangiocytes of cirrhotic rats appear to be more tolerant to ischemia of bile duct than non-cirrhotic rats. This may be due to the protective role of arterioportal fistulas.
authors.affiliation: Department of Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
authors.forename: Dong-Zheng
authors.initials: DZ
authors.lastname: Li
authors.forename: Jun
authors.initials: J
authors.lastname: Jiang
authors.forename: Yi
authors.initials: Y
authors.lastname: Miao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001164:Arteriovenous Fistula / Q000503:physiopathology*; D001652:Bile Ducts / Q000098:blood supply* / Q000473:pathology* / Q000503:physiopathology; D001775:Blood Circulation / Q000502:physiology; D004195:Disease Models, Animal; D004853:Epoxy Resins; D051793:Hypoxia-Inducible Factor 1 / Q000378:metabolism; D007511:Ischemia / Q000473:pathology* / Q000503:physiopathology; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008103:Liver Cirrhosis / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D004853:Epoxy Resins; D051793:Hypoxia-Inducible Factor 1; D016328:NF-kappa B; D042461:Vascular Endothelial Growth Factor A