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

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy. / Iversen, Peter; 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, 2009, p. 863-871.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

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, vol. 136, no. 3, pp. 863-871. https://doi.org/10.1053/j.gastro.2008.10.057

APA

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

Vancouver

Iversen P, Bak LK, Waagepetersen HS, Vafaee MS, Borghammer P, Mouridsen K et al. Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy. Gastroenterology. 2009;136(3):863-871. https://doi.org/10.1053/j.gastro.2008.10.057

Author

Iversen, Peter ; 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.

Bibtex

@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",

}

RIS

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

VL - 136

SP - 863

EP - 871

JO - Gastroenterology

JF - Gastroenterology

SN - 0016-5085

IS - 3

ER -

ID: 10487781