The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo

Publikation: Bidrag til bog/antologi/rapportBidrag til bog/antologiForskningfagfællebedømt

Standard

The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo. / Hasselbalch, Steen; Paulson, Olaf Bjarne.

Neural Metabolism In Vivo. red. / In-Young Choi; Rolf Gruetter. Bind 4 2012. s. 417-432.

Publikation: Bidrag til bog/antologi/rapportBidrag til bog/antologiForskningfagfællebedømt

Harvard

Hasselbalch, S & Paulson, OB 2012, The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo. i I-Y Choi & R Gruetter (red), Neural Metabolism In Vivo. bind 4, s. 417-432. https://doi.org/10.1007/978-1-4614-1788-0_14

APA

Hasselbalch, S., & Paulson, O. B. (2012). The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo. I I-Y. Choi, & R. Gruetter (red.), Neural Metabolism In Vivo (Bind 4, s. 417-432) https://doi.org/10.1007/978-1-4614-1788-0_14

Vancouver

Hasselbalch S, Paulson OB. The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo. I Choi I-Y, Gruetter R, red., Neural Metabolism In Vivo. Bind 4. 2012. s. 417-432 https://doi.org/10.1007/978-1-4614-1788-0_14

Author

Hasselbalch, Steen ; Paulson, Olaf Bjarne. / The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo. Neural Metabolism In Vivo. red. / In-Young Choi ; Rolf Gruetter. Bind 4 2012. s. 417-432

Bibtex

@inbook{c5cd5d4cbbd045218971108fd0bcf0ff,
title = "The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo",
abstract = "The energy supplied to the brain by metabolic substrate is largely utilized for maintaining synaptic transmission. In this regulation cerebral blood flow and glucose consumption is tightly coupled as well in the resting condition as during activation. Quantification of cerebral blood flow and metabolism was originally performed using the Kety-Schmidt method and this method still represent the gold standard by which subsequent methods have been evaluated. However, in its classical setting, the method overestimates cerebral blood flow. Studies of metabolic changes during activation must take this into account, and subsequent methods for measurement of regional glucose metabolism must be corrected accordingly in order to allow reliable quantitative comparisons of metabolite changes in activation studies. For studies of regional metabolic changes during activation quantification poses further difficulties due to limitation in resolution and partial volume effects.In contrast to the tight coupling between regional glucose metabolism and cerebral blood flow, there is an uncoupling between flow and oxygen consumption as the latter only increases to a limited extend. The excess glucose uptake is thus not used for aerobic metabolism. Although some of the excess glucose uptake can be explained by lactate production, this phenomenon can still not account for the excess glucose uptake. Thus, more complex metabolic patterns in the brain might be reflected in the excess glucose uptake during activation, and especially temporal relationships must be taken into account.What triggers the flow increase during functional brain activation is not entirely elucidated. The demand for excess glucose uptake may be important and a possible oxygen deficit in tissue distant from the capillaries is probably of minor importance. The mechanism by which cerebral blood flow increases during activation may incorporate changes in glycolytic substrates or local changes in astrocytes or neurons that triggers the production of vasoactive substances.",
author = "Steen Hasselbalch and Paulson, {Olaf Bjarne}",
year = "2012",
doi = "10.1007/978-1-4614-1788-0_14",
language = "English",
isbn = "978-1-4614-1787-3",
volume = "4",
pages = "417--432",
editor = "In-Young Choi and Rolf Gruetter",
booktitle = "Neural Metabolism In Vivo",

}

RIS

TY - CHAP

T1 - The Coupling of Cerebral Metabolic Rate of Glucose and Cerebral Blood Flow In Vivo

AU - Hasselbalch, Steen

AU - Paulson, Olaf Bjarne

PY - 2012

Y1 - 2012

N2 - The energy supplied to the brain by metabolic substrate is largely utilized for maintaining synaptic transmission. In this regulation cerebral blood flow and glucose consumption is tightly coupled as well in the resting condition as during activation. Quantification of cerebral blood flow and metabolism was originally performed using the Kety-Schmidt method and this method still represent the gold standard by which subsequent methods have been evaluated. However, in its classical setting, the method overestimates cerebral blood flow. Studies of metabolic changes during activation must take this into account, and subsequent methods for measurement of regional glucose metabolism must be corrected accordingly in order to allow reliable quantitative comparisons of metabolite changes in activation studies. For studies of regional metabolic changes during activation quantification poses further difficulties due to limitation in resolution and partial volume effects.In contrast to the tight coupling between regional glucose metabolism and cerebral blood flow, there is an uncoupling between flow and oxygen consumption as the latter only increases to a limited extend. The excess glucose uptake is thus not used for aerobic metabolism. Although some of the excess glucose uptake can be explained by lactate production, this phenomenon can still not account for the excess glucose uptake. Thus, more complex metabolic patterns in the brain might be reflected in the excess glucose uptake during activation, and especially temporal relationships must be taken into account.What triggers the flow increase during functional brain activation is not entirely elucidated. The demand for excess glucose uptake may be important and a possible oxygen deficit in tissue distant from the capillaries is probably of minor importance. The mechanism by which cerebral blood flow increases during activation may incorporate changes in glycolytic substrates or local changes in astrocytes or neurons that triggers the production of vasoactive substances.

AB - The energy supplied to the brain by metabolic substrate is largely utilized for maintaining synaptic transmission. In this regulation cerebral blood flow and glucose consumption is tightly coupled as well in the resting condition as during activation. Quantification of cerebral blood flow and metabolism was originally performed using the Kety-Schmidt method and this method still represent the gold standard by which subsequent methods have been evaluated. However, in its classical setting, the method overestimates cerebral blood flow. Studies of metabolic changes during activation must take this into account, and subsequent methods for measurement of regional glucose metabolism must be corrected accordingly in order to allow reliable quantitative comparisons of metabolite changes in activation studies. For studies of regional metabolic changes during activation quantification poses further difficulties due to limitation in resolution and partial volume effects.In contrast to the tight coupling between regional glucose metabolism and cerebral blood flow, there is an uncoupling between flow and oxygen consumption as the latter only increases to a limited extend. The excess glucose uptake is thus not used for aerobic metabolism. Although some of the excess glucose uptake can be explained by lactate production, this phenomenon can still not account for the excess glucose uptake. Thus, more complex metabolic patterns in the brain might be reflected in the excess glucose uptake during activation, and especially temporal relationships must be taken into account.What triggers the flow increase during functional brain activation is not entirely elucidated. The demand for excess glucose uptake may be important and a possible oxygen deficit in tissue distant from the capillaries is probably of minor importance. The mechanism by which cerebral blood flow increases during activation may incorporate changes in glycolytic substrates or local changes in astrocytes or neurons that triggers the production of vasoactive substances.

U2 - 10.1007/978-1-4614-1788-0_14

DO - 10.1007/978-1-4614-1788-0_14

M3 - Book chapter

SN - 978-1-4614-1787-3

VL - 4

SP - 417

EP - 432

BT - Neural Metabolism In Vivo

A2 - Choi, In-Young

A2 - Gruetter, Rolf

ER -

ID: 48461163