No oxygen delivery limitation in hepatic encephalopathy

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No oxygen delivery limitation in hepatic encephalopathy. / Gjedde, Albert; Keiding, Susanne; Vilstrup, Hendrik; Iversen, Peter.

In: Metabolic Brain Disease, Vol. 25, No. 1, 2010, p. 57-63.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Gjedde, A, Keiding, S, Vilstrup, H & Iversen, P 2010, 'No oxygen delivery limitation in hepatic encephalopathy', Metabolic Brain Disease, vol. 25, no. 1, pp. 57-63. https://doi.org/10.1007/s11011-010-9179-9

APA

Gjedde, A., Keiding, S., Vilstrup, H., & Iversen, P. (2010). No oxygen delivery limitation in hepatic encephalopathy. Metabolic Brain Disease, 25(1), 57-63. https://doi.org/10.1007/s11011-010-9179-9

Vancouver

Gjedde A, Keiding S, Vilstrup H, Iversen P. No oxygen delivery limitation in hepatic encephalopathy. Metabolic Brain Disease. 2010;25(1):57-63. https://doi.org/10.1007/s11011-010-9179-9

Author

Gjedde, Albert ; Keiding, Susanne ; Vilstrup, Hendrik ; Iversen, Peter. / No oxygen delivery limitation in hepatic encephalopathy. In: Metabolic Brain Disease. 2010 ; Vol. 25, No. 1. pp. 57-63.

Bibtex

@article{377a54c089c911df928f000ea68e967b,
title = "No oxygen delivery limitation in hepatic encephalopathy",
abstract = "Hepatic encephalopathy is a condition of reduced brain functioning in which both blood flow and brain energy metabolism declined. It is not known whether blood flow or metabolism is the primary limiting factor of brain function in this condition. We used calculations of mitochondrial oxygen tension to choose between cause and effect in three groups of volunteers, including healthy control subjects (HC), patients with cirrhosis of the liver without hepatic encephalopathy (CL), and patients with cirrhosis with acute hepatic encephalopathy. Compared to HC subjects, blood flow and energy metabolism had declined in all gray matter regions of the brain in patients with HE but not significantly in patients with CL. Analysis of flow-metabolism coupling indicated that blood flow declined in HE as a consequence of reduced brain energy metabolism implied by the calculation of increased mitochondrial oxygen tensions that patients with HE were unable to utilize. We ascribe the inability to use the delivered oxygen of patients with HE to a specific inhibition associated with oxidative metabolism in mitochondria.",
author = "Albert Gjedde and Susanne Keiding and Hendrik Vilstrup and Peter Iversen",
note = "Keywords: Aged; Basal Metabolism; Brain; Cerebrovascular Circulation; Energy Metabolism; Female; Fibrosis; Hepatic Encephalopathy; Humans; Male; Middle Aged; Mitochondria; Oxygen; Oxygen Consumption",
year = "2010",
doi = "10.1007/s11011-010-9179-9",
language = "English",
volume = "25",
pages = "57--63",
journal = "Metabolic Brain Disease",
issn = "0885-7490",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - No oxygen delivery limitation in hepatic encephalopathy

AU - Gjedde, Albert

AU - Keiding, Susanne

AU - Vilstrup, Hendrik

AU - Iversen, Peter

N1 - Keywords: Aged; Basal Metabolism; Brain; Cerebrovascular Circulation; Energy Metabolism; Female; Fibrosis; Hepatic Encephalopathy; Humans; Male; Middle Aged; Mitochondria; Oxygen; Oxygen Consumption

PY - 2010

Y1 - 2010

N2 - Hepatic encephalopathy is a condition of reduced brain functioning in which both blood flow and brain energy metabolism declined. It is not known whether blood flow or metabolism is the primary limiting factor of brain function in this condition. We used calculations of mitochondrial oxygen tension to choose between cause and effect in three groups of volunteers, including healthy control subjects (HC), patients with cirrhosis of the liver without hepatic encephalopathy (CL), and patients with cirrhosis with acute hepatic encephalopathy. Compared to HC subjects, blood flow and energy metabolism had declined in all gray matter regions of the brain in patients with HE but not significantly in patients with CL. Analysis of flow-metabolism coupling indicated that blood flow declined in HE as a consequence of reduced brain energy metabolism implied by the calculation of increased mitochondrial oxygen tensions that patients with HE were unable to utilize. We ascribe the inability to use the delivered oxygen of patients with HE to a specific inhibition associated with oxidative metabolism in mitochondria.

AB - Hepatic encephalopathy is a condition of reduced brain functioning in which both blood flow and brain energy metabolism declined. It is not known whether blood flow or metabolism is the primary limiting factor of brain function in this condition. We used calculations of mitochondrial oxygen tension to choose between cause and effect in three groups of volunteers, including healthy control subjects (HC), patients with cirrhosis of the liver without hepatic encephalopathy (CL), and patients with cirrhosis with acute hepatic encephalopathy. Compared to HC subjects, blood flow and energy metabolism had declined in all gray matter regions of the brain in patients with HE but not significantly in patients with CL. Analysis of flow-metabolism coupling indicated that blood flow declined in HE as a consequence of reduced brain energy metabolism implied by the calculation of increased mitochondrial oxygen tensions that patients with HE were unable to utilize. We ascribe the inability to use the delivered oxygen of patients with HE to a specific inhibition associated with oxidative metabolism in mitochondria.

U2 - 10.1007/s11011-010-9179-9

DO - 10.1007/s11011-010-9179-9

M3 - Journal article

C2 - 20182779

VL - 25

SP - 57

EP - 63

JO - Metabolic Brain Disease

JF - Metabolic Brain Disease

SN - 0885-7490

IS - 1

ER -

ID: 20688652