Metabolic Control of Resting Hemispheric Cerebral Blood Flow is Oxidative, not Glycolytic

Author:

Powers William J1,Videen Tom O23,Markham Joanne3,Walter Vonn4,Perlmutter Joel S5

Affiliation:

1. Department of Neurology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA

2. Department of Neurology, Washington University, School of Medicine, St Louis, Missouri, USA

3. Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, Missouri, USA

4. Department of Biostatistics and the Lineberger Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA

5. Departments of Neurology, Anatomy and Neurobiology, Program in Physical Therapy, Program in Occupational Therapy and the Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, Missouri, USA

Abstract

Although the close regional coupling of resting cerebral blood flow (CBF) with both cerebral metabolic rate of oxygen (CMRO2) and cerebral metabolic rate of glucose (CMRglc) within individuals is well documented, there are few data regarding the coupling between whole brain flow and metabolism among different subjects. To investigate the metabolic control of resting whole brain CBF, we performed multivariate analysis of hemispheric CMRO2, CMRglc, and other covariates as predictors of resting CBF among 23 normal humans. The univariate analysis showed that only CMRO2 was a significant predictor of CBF. The final multivariate model contained two additional terms in addition to CMRO2: arterial oxygen content and oxygen extraction fraction. Notably, arterial plasma glucose concentration and CMRglc were not included in the final model. Our data demonstrate that the metabolic factor controlling hemispheric CBF in the normal resting brain is CMRO2 and that CMRglc does not make a contribution. Our findings provide evidence for compartmentalization of brain metabolism into a basal component in which CBF is coupled to oxygen metabolism and an activation component in which CBF is controlled by another mechanism.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Clinical Neurology,Neurology

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