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 - 2010/3
Y1 - 2010/3
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
SN - 0885-7490
VL - 25
SP - 57
EP - 63
JO - Metabolic Brain Disease
JF - Metabolic Brain Disease
IS - 1
ER -