title: Impact of hepatic vein deprivation on liver regeneration and function after major hepatectomy.
abstract: OBJECTIVE
  In extended liver resections, the preservation of vascular and biliary structures of the entire remnant liver is of paramount importance. The impact of venous outflow impairment and its consequences for liver regeneration and function are still a matter of debate.
  
  
  METHODS
  Rats (n = 75) were subjected to a 90% partial hepatectomy (PH), to a 70% liver resection with narrowing of the hepatic outflow of an additional 20% parenchyma (70%+ PH) or to an anatomic 70% PH. Postoperatively hepatocyte proliferation (Ki-67), liver function and survival were assessed. Gene expression analysis for markers of regeneration was determined by in-house complementary (DNA) arrays and quantitative real-time polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  Ninety percent PH led to a greater regenerative response as shown Ki-67 compared to animals with a 70%+PH (p < 0.05). However, liver function was equally impaired in both groups. Rats with 70% PH showed a greater proliferation index with less hepatic injury and better liver function. While mortality was 0% in the group of 70% PH, rats with 90% PH and 70+PH had a reduced survival of 75% (p < 0.05)
  
  
  CONCLUSIONS
  Venous outflow obstruction leads to an impairment of liver regeneration and liver function. In cases with critically small liver remnants, restoration of an adequate venous outflow may be mandatory.
authors.affiliation: Department of General, Visceral and Transplantation Surgery, University Hospital Essen, Essen, Germany. maximilian.bockhorn@uk-essen.de
authors.forename: Maximilian
authors.initials: M
authors.lastname: Bockhorn
authors.forename: Tamasz
authors.initials: T
authors.lastname: Benkö
authors.forename: Bettina
authors.initials: B
authors.lastname: Opitz
authors.forename: Sien-Yi
authors.initials: SY
authors.lastname: Sheu
authors.forename: Georgios C
authors.initials: GC
authors.lastname: Sotiropoulos
authors.forename: Jörg F
authors.initials: JF
authors.lastname: Schlaak
authors.forename: Christoph E
authors.initials: CE
authors.lastname: Broelsch
authors.forename: Hauke
authors.initials: H
authors.lastname: Lang
mesh_terms: D000818:Animals; D001835:Body Weight; D015870:Gene Expression / Q000235:genetics; D006498:Hepatectomy / Q000379:methods*; D006503:Hepatic Veins / Q000601:surgery*; D022781:Hepatocytes / Q000473:pathology; D053592:Interleukin-1 Receptor-Associated Kinases / Q000235:genetics; D019394:Ki-67 Antigen / Q000032:analysis; D008099:Liver / Q000473:pathology; D008111:Liver Function Tests; D008115:Liver Regeneration / Q000235:genetics / Q000502:physiology*; D008297:Male; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D020574:Proto-Oncogene Proteins c-sis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D000077293:Receptor, Transforming Growth Factor-beta Type I; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016019:Survival Analysis
chemical_list: D019394:Ki-67 Antigen; D020574:Proto-Oncogene Proteins c-sis; D018125:Receptors, Transforming Growth Factor beta; D053592:Interleukin-1 Receptor-Associated Kinases; D017346:Protein Serine-Threonine Kinases; D000077293:Receptor, Transforming Growth Factor-beta Type I; C000625843:Tgfbr1 protein, rat