Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy

Peter Iversen, Michael Sørensen, Lasse Kristoffer Bak, Helle Sønderby Waagepetersen, Manouchehr Seyedi Vafaee, Per Borghammer, Kim Mouridsen, Svend Borup Jensen, Hendrik Vilstrup, Arne Schousboe, Peter Ott, Albert Gjedde, Susanne Keiding

Research output: Contribution to journalArticle

Abstract

Background & Aims: It is unclear whether patients with hepatic encephalopathy (HE) have disturbed brain oxygen metabolism and blood flow. Methods: We measured cerebral oxygen metabolism rate (CMRO2) by using 15O-oxygen positron emission tomography (PET); and cerebral blood flow (CBF) by using 15O-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 CMRO2 nor CBF differed significantly between cirrhotic patients without HE and healthy subjects, but were both significantly reduced in cirrhotic patients with HE (P <.01). CMRO2 was 0.96 ± 0.07 μmol 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. CMRO2 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 CMRO2 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.

Original languageEnglish (US)
Pages (from-to)863-871
Number of pages9
JournalGastroenterology
Volume136
Issue number3
DOIs
StatePublished - Mar 2009
Externally publishedYes

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Hepatic Encephalopathy
Oxygen Consumption
Fibrosis
Cerebrovascular Circulation
Healthy Volunteers
Oxygen
Brain
Ammonia
Positron-Emission Tomography
Liver Cirrhosis
Energy Metabolism
Magnetic Resonance Spectroscopy

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Iversen, P., Sørensen, M., Bak, L. K., Waagepetersen, H. S., Vafaee, M. S., Borghammer, P., ... Keiding, S. (2009). Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy. Gastroenterology, 136(3), 863-871. https://doi.org/10.1053/j.gastro.2008.10.057

Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy. / Iversen, Peter; Sørensen, Michael; Bak, Lasse Kristoffer; Waagepetersen, Helle Sønderby; Vafaee, Manouchehr Seyedi; Borghammer, Per; Mouridsen, Kim; Jensen, Svend Borup; Vilstrup, Hendrik; Schousboe, Arne; Ott, Peter; Gjedde, Albert; Keiding, Susanne.

In: Gastroenterology, Vol. 136, No. 3, 03.2009, p. 863-871.

Research output: Contribution to journalArticle

Iversen, P, Sørensen, M, Bak, LK, Waagepetersen, HS, Vafaee, MS, Borghammer, P, Mouridsen, K, Jensen, SB, Vilstrup, H, Schousboe, A, Ott, P, Gjedde, A & Keiding, S 2009, 'Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy', Gastroenterology, vol. 136, no. 3, pp. 863-871. https://doi.org/10.1053/j.gastro.2008.10.057
Iversen, Peter ; Sørensen, Michael ; Bak, Lasse Kristoffer ; Waagepetersen, Helle Sønderby ; Vafaee, Manouchehr Seyedi ; Borghammer, Per ; Mouridsen, Kim ; Jensen, Svend Borup ; Vilstrup, Hendrik ; Schousboe, Arne ; Ott, Peter ; Gjedde, Albert ; Keiding, Susanne. / Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy. In: Gastroenterology. 2009 ; Vol. 136, No. 3. pp. 863-871.
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T1 - Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy

AU - Iversen, Peter

AU - Sørensen, Michael

AU - Bak, Lasse Kristoffer

AU - Waagepetersen, Helle Sønderby

AU - Vafaee, Manouchehr Seyedi

AU - Borghammer, Per

AU - Mouridsen, Kim

AU - Jensen, Svend Borup

AU - Vilstrup, Hendrik

AU - Schousboe, Arne

AU - Ott, Peter

AU - Gjedde, Albert

AU - Keiding, Susanne

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Y1 - 2009/3

N2 - Background & Aims: It is unclear whether patients with hepatic encephalopathy (HE) have disturbed brain oxygen metabolism and blood flow. Methods: We measured cerebral oxygen metabolism rate (CMRO2) by using 15O-oxygen positron emission tomography (PET); and cerebral blood flow (CBF) by using 15O-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 CMRO2 nor CBF differed significantly between cirrhotic patients without HE and healthy subjects, but were both significantly reduced in cirrhotic patients with HE (P <.01). CMRO2 was 0.96 ± 0.07 μmol 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. CMRO2 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 CMRO2 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.

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