PERSISTENT RESETTING OF THE CEREBRAL OXYGEN GLUCOSE-UPTAKE RATIO BY BRAIN ACTIVATION - EVIDENCE OBTAINED WITH THE KETY-SCHMIDT TECHNIQUE

Citation
Pl. Madsen et al., PERSISTENT RESETTING OF THE CEREBRAL OXYGEN GLUCOSE-UPTAKE RATIO BY BRAIN ACTIVATION - EVIDENCE OBTAINED WITH THE KETY-SCHMIDT TECHNIQUE, Journal of cerebral blood flow and metabolism, 15(3), 1995, pp. 485-491
Citations number
22
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism",Hematology
ISSN journal
0271678X
Volume
15
Issue
3
Year of publication
1995
Pages
485 - 491
Database
ISI
SICI code
0271-678X(1995)15:3<485:PROTCO>2.0.ZU;2-E
Abstract
Global cerebral blood flow (CBF), global cerebral metabolic rates for oxygen (CMRO(2)), and for glucose (CMR(glc)), and lactate efflux were measured during rest and during cerebral activation induced by the Wis consin card sorting test. Measurements were performed in healthy volun teers using the Kety-Schmidt technique. Global CMRO(2) was unchanged d uring cerebral activation, whereas global CBF and global CMR(glc) both increased by 12%, reducing the molar ratio of oxygen to glucose consu mption from 6.0 during baseline conditions to 5.4 during activation, D ata obtained in the period following cerebral activation showed that t he activation-induced resetting of the relation between CMR(glc) and C MRO(2) persisted virtually unaltered for greater than or equal to 40 m in after the mental activation task was terminated. The activation-ind uced increase in cerebral lactate efflux measured over the same time p eriod accounted for only a small fraction of the activation-induced ex cess glucose uptake. These data confirm earlier reports that brain act ivation can induce resetting of the cerebral oxygen/glucose consumptio n ratio, and indicate that the resetting persists for a long period af ter cerebral activation has been terminated and physiologic stress ind icators returned to baseline values. Activation-induced resetting of t he cerebral oxygen/glucose uptake ratio is not necessarily accounted f or by increased lactate production from nonoxidative glucose metabolis m.