Cerebral Blood Flow Response to Functional Activation

Cerebral blood flow (CBF) and cerebral metabolic rate are normally coupled, that is an increase in metabolic demand will lead to an increase in flow. However, during functional activation, CBF and glucose metabolism remain coupled as they increase in proportion, whereas oxygen metabolism only increa...

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Vydané v:Journal of cerebral blood flow and metabolism Ročník 30; číslo 1; s. 2 - 14
Hlavní autori: Paulson, Olaf B, Hasselbalch, Steen G, Rostrup, Egill, Knudsen, Gitte Moos, Pelligrino, Dale
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London, England SAGE Publications 01.01.2010
Nature Publishing Group
Sage Publications Ltd
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ISSN:0271-678X, 1559-7016, 1559-7016
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Shrnutí:Cerebral blood flow (CBF) and cerebral metabolic rate are normally coupled, that is an increase in metabolic demand will lead to an increase in flow. However, during functional activation, CBF and glucose metabolism remain coupled as they increase in proportion, whereas oxygen metabolism only increases to a minor degree—the so-called uncoupling of CBF and oxidative metabolism. Several studies have dealt with these issues, and theories have been forwarded regarding the underlying mechanisms. Some reports have speculated about the existence of a potentially deficient oxygen supply to the tissue most distant from the capillaries, whereas other studies point to a shift toward a higher degree of non-oxidative glucose consumption during activation. In this review, we argue that the key mechanism responsible for the regional CBF (rCBF) increase during functional activation is a tight coupling between rCBF and glucose metabolism. We assert that uncoupling of rCBF and oxidative metabolism is a consequence of a less pronounced increase in oxygen consumption. On the basis of earlier studies, we take into consideration the functional recruitment of capillaries and attempt to accommodate the cerebral tissue's increased demand for glucose supply during neural activation with recent evidence supporting a key function for astrocytes in rCBF regulation.
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ISSN:0271-678X
1559-7016
1559-7016
DOI:10.1038/jcbfm.2009.188