Regulation of cerebral oxygen delivery.

Abstract

Under normal conditions, it is generally accepted that for the adult mammalian cortex, almost all the energy required for cerebral ATP generation is supplied by oxidation of glucose through the tri-carboxylic acid cycle (Siesjo, 1978), and cerebral metabolic rates of oxygen and glucose use (i.e., CMRO2 and CMRglc, respectively) are regionally modified to fulfil metabolic needs through regulation of cerebral blood flow (CBF) and volume (CBV) (Roy and Sherrington, 1890). However, some positron emission tomography (PET) results have reported that during brain activation of awake humans CBF increases by a greater fraction than CMRO2 (Fox and Raichle, 1986; Fox et al., 1988). In the last few decades, ever since in vivo cortical measurements could be made of CBF and/or CMRO2, the mechanisms for the proportionality of changes between CBF and CMRO2 due to physiological perturbations have remained intangible, and the measured stoichiometries have varied reflecting a variety of experimental methods and/or conditions. However, regionally tight relationship between CMRO2 and CBF has been observed at rest with a ratio of about ~1:1 (Kety et al., 1947–8; Raichle et al., 1976).