title: Low cerebral oxygen consumption and blood flow in patients with cirrhosis and an acute episode of hepatic encephalopathy.
abstract: OBJECTIVE
  It is unclear whether patients with hepatic encephalopathy (HE) have disturbed brain oxygen metabolism and blood flow.
  
  
  METHODS
  We measured cerebral oxygen metabolism rate (CMRO(2)) by using (15)O-oxygen positron emission tomography (PET); and cerebral blood flow (CBF) by using (15)O-water PET in 6 patients with liver cirrhosis and an acute episode of overt HE, 6 cirrhotic patients without HE, and 7 healthy subjects.
  
  
  RESULTS
  Neither whole-brain CMRO(2) nor CBF differed significantly between cirrhotic patients without HE and healthy subjects, but were both significantly reduced in cirrhotic patients with HE (P < .01). CMRO(2) was 0.96 +/- 0.07 mumol oxygen/mL brain tissue/min (mean +/- SEM) in cirrhotic patients with HE, 1.34 +/- 0.08 in cirrhotic patients without HE, and 1.35 +/- 0.05 in healthy subjects; and CBF was 0.29 +/- 0.01 mL blood/mL brain tissue/min in patients with HE, 0.47 +/- 0.02 in patients without HE, and 0.49 +/- 0.03 in healthy subjects. CMRO(2) and CBF were correlated, and both variables correlated negatively with arterial ammonia concentration. Analysis of regional values, using individual magnetic resonance co-registrations, showed that the reductions in CMRO(2) and CBF in patients with HE were essentially generalized throughout the brain.
  
  
  CONCLUSIONS
  The observations imply that reduced cerebral oxygen consumption and blood flow in cirrhotic patients with an acute episode of overt HE are associated with HE and not cirrhosis as such, and that the primary event in the pathogenesis of HE could be inhibition of cerebral energy metabolism by increased blood ammonia.
authors.affiliation: PET Centre, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Peter
authors.initials: P
authors.lastname: Iversen
authors.forename: Michael
authors.initials: M
authors.lastname: Sørensen
authors.forename: Lasse Kristoffer
authors.initials: LK
authors.lastname: Bak
authors.forename: Helle Sønderby
authors.initials: HS
authors.lastname: Waagepetersen
authors.forename: Manouchehr Seyedi
authors.initials: MS
authors.lastname: Vafaee
authors.forename: Per
authors.initials: P
authors.lastname: Borghammer
authors.forename: Kim
authors.initials: K
authors.lastname: Mouridsen
authors.forename: Svend Borup
authors.initials: SB
authors.lastname: Jensen
authors.forename: Hendrik
authors.initials: H
authors.lastname: Vilstrup
authors.forename: Arne
authors.initials: A
authors.lastname: Schousboe
authors.forename: Peter
authors.initials: P
authors.lastname: Ott
authors.forename: Albert
authors.initials: A
authors.lastname: Gjedde
authors.forename: Susanne
authors.initials: S
authors.lastname: Keiding
mesh_terms: D000208:Acute Disease; D000368:Aged; D001921:Brain / Q000098:blood supply / Q000000981:diagnostic imaging / Q000378:metabolism; D002560:Cerebrovascular Circulation; D005260:Female; D019788:Fluorodeoxyglucose F18; D006501:Hepatic Encephalopathy / Q000000981:diagnostic imaging* / Q000378:metabolism*; D006801:Humans; D008103:Liver Cirrhosis / Q000000981:diagnostic imaging* / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010104:Oxygen Radioisotopes; D049268:Positron-Emission Tomography
chemical_list: D010104:Oxygen Radioisotopes; D019788:Fluorodeoxyglucose F18; D010100:Oxygen