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

Peter Iversen; 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

doi: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

Peter Iversen, 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

Institut for Neurovidenskab

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

92 Citationer (Scopus)

Abstract

Udgivelsesdato: Marts

Originalsprog	Engelsk
Tidsskrift	Gastroenterology
Vol/bind	136
Udgave nummer	3
Sider (fra-til)	863-871
ISSN	0016-5085
DOI	https://doi.org/10.1053/j.gastro.2008.10.057
Status	Udgivet - 2009

Adgang til dokumentet

10.1053/j.gastro.2008.10.057

Citationsformater

Iversen, P., Bak, L. K., Waagepetersen, H. S., Vafaee, M. S., Borghammer, P., Mouridsen, K., Jensen, S. B., 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, 136(3), 863-871. https://doi.org/10.1053/j.gastro.2008.10.057

Iversen, P, 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, bind 136, nr. 3, s. 863-871. https://doi.org/10.1053/j.gastro.2008.10.057

@article{45229ad0f91811ddb219000ea68e967b,

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

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 (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.",

author = "Peter Iversen and Bak, {Lasse Kristoffer} and Waagepetersen, {Helle S{\o}nderby} and Vafaee, {Manouchehr Seyedi} and Per Borghammer and Kim Mouridsen and Jensen, {Svend Borup} and Hendrik Vilstrup and Arne Schousboe and Peter Ott and Albert Gjedde and Susanne Keiding",

year = "2009",

doi = "10.1053/j.gastro.2008.10.057",

language = "English",

volume = "136",

pages = "863--871",

journal = "Gastroenterology",

issn = "0016-5085",

publisher = "Elsevier",

number = "3",

}

TY - JOUR

T1 - Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy

AU - Iversen, Peter

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

PY - 2009

Y1 - 2009

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 (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.

AB - 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 (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.

U2 - 10.1053/j.gastro.2008.10.057

DO - 10.1053/j.gastro.2008.10.057

M3 - Journal article

C2 - 19041869

SN - 0016-5085

VL - 136

SP - 863

EP - 871

JO - Gastroenterology

JF - Gastroenterology

IS - 3

ER -