Localization of Functional Activity in the Central Nervous System by Measurement of Glucose Utilization with Radioactive Deoxyglucose

Uncoupled Cerebral Blood Flow and Metabolism after Severe Global Ischemia in Rats

“…CBF and CMR02 may be coupled early postischemia with subsequent deterioration in mi tochondrial function and uncoupling of CBF and CMR02 beginning about 3-4 h after severe GBI. Although the precise mechanisms involved in the coupling of CBF with CMR remain to be deter mined, locally released metabolites (H +, adeno sine, eicosanoids, neurotransmitters) and extrinsic factors (autonomic tone, input from remote brain areas) are involved (Sokoloff, 1981;Tanaka et al, 1985;Dietrich et al, 1986;Chemtob et al, 1990). The mechanism of the progression of hypo perfusion to relative or absolute hyperemia despite sustained postischemic oxidative hypometabolism remains unknown.…”

Regional Alterations in Glucose Consumption and Metabolite Levels during Postischemic Recovery in Cat Brain

“…the similarity of the rate con stants between rat and monkey (Kennedy et aI., 1978) suggests that they may be similar in cat brain. Therefore, an "uncorrected" LCMRgl was calculated by using the LC determined for the normal anesthetized cat (0.411) (Sokoloff, 1981) and using the rate constants for 2DG and glucose in the normal rat (Sokoloff et aI., 1977;Sa vaki et aI., 1980). However, since an alteration of LC and the rate constants could have occurred in this particular model, possible alterations in these parameters were es timated in each tissue sample.…”

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Summary: Local CMRgl (LCMRgl) and metabolite levels were measured in the same tissue samples fol lowing 4 h of recirculation after 1 h of occlusion of the middle cerebral artery in the caL The rate of glucose utilization was calculated using direct measurement of tissue deoxyglucose-6-phosphate and using a "lumped" constant corrected in each sample for alterations in tissue glucose, Increased LCMRgl (compared with that in sham operated animals) occurred in regions with only minor alterations in levels of lactate and phosphocreatine, By contrast, LCMRgl was markedly depressed in regions Glucose is the principal substrate for energy me tabolism in brain, Measurement of the local CMRgl (LCMRgl) using the radiolabeled glucose analogue [ l4 C]2-deoxyglucose ([ l4 C]2DG) has been a valuable method for evaluating functional activity of brain tissue (Sokoloff, 1981;Greenberg and Reivich, 1983). Among numerous applications of this tech nique, there have been several reports showing a broad spectrum of changes in LCMRgl in animal studies of ischemia, ranging from marked inhibition to pronounced activation (Ginsberg et ai., 1977;Diemer and Siemkowicz, 1980; Welsh et ai., 1980a; Pulsinelli et ai., 1982; Choki et aI., 1983).

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Use of 2-Deoxy-D[1-11C]Glucose for the Determination of Local Cerebral Glucose Metabolism in Humans: Variation within and between Subjects

“…glucose metabolism in normal and altered states Sokoloff, 1981). Recently it has been possible to extend this type of study to humans using 18F-2-deoxy-2-fluoro-D-glucose (1SF-FDG), as the tracer and positron emission to mography to quantitate the radioactivity concen tration in discrete volumes of brain tissue Reivich et al , 1979).…”