Time-Dependent Changes of Lumped and Rate Constants in the Deoxyglucose Method in Experimental Cerebral Ischemia

Abstract

Time-dependent changes in the lumped and rate constants in a bilateral middle cerebral artery (MCA) occlusion in cats were evaluated. These variables were measured in 11 cats after a sham operation, in five after a 1-h occlusion, in two after a 2-h occlusion, in five after a 4-h occlusion, and in four after a 16-h occlusion. The time course of the cerebral tissue radioactivity [Ci* (t)] was monitored by external coincidence counting during a programmed infusion of [18F]2-fluorodeoxyglucose (FDG). Arterial plasma concentration [Cp* (t)] of tracer was kept constant during the first 45 min. Comparison of k2* and k3* in the sham-operated group, estimated by external coincidence counting, and by the ratio of extraction fractions of glucose and [18F]2-FDG, demonstrated no significant difference between these rate constants in these two groups of animals. The rate and lumped constants were also estimated from Ci* (t) and Cp* (t), as well as from the ratio of extraction fractions of glucose and [18F]2-FDG, respectively, in the MCA occlusion group. Significant decrease in k3* was observed after 1 h of occlusion (20% lower than in the sham operation, p less than 0.05); in k1* decrease occurred within 4 h of occlusion (21% lower than in the sham operation, p less than 0.05). However, decrease in k2* was observed only after 16 h of occlusion (26% lower than in the sham operation, p less than 0.05). Namely, decrease of rate constants occurred first in k3* then in k1* and k2*.(ABSTRACT TRUNCATED AT 250 WORDS)

Transient Focal Increase in Perihematomal Glucose Metabolism After Acute Human Intracerebral Hemorrhage

“…In adults, the lumped constant has been shown to change appreciably only in tumors or under conditions in which glucose delivery becomes rate limiting for glucose metabolism, eg, during ischemia and hypoglycemia. [12][13][14] We have previously shown that perihematomal ischemia is not present after acute ICH. 15 None of the subjects experienced hypoglycemia over the study period.…”

Selective defect of in vivo glycolysis in early Huntington's disease striatum

“…In measuring CMRglc with [ 18 F]fluorodeoxyglucose ( 18 FDG), we explicitly assumed that the lumped constant (LC) value is the same for HD as it is for normal controls. In adults, the LC has been shown to change appreciably only in tumors or under conditions in which glucose delivery becomes rate limiting for glucose metabolism, e.g., during ischemia and hypoglycemia (23)(24)(25)(26). In our participants with HD, neither ischemia nor hypoglycemia was present.…”

Increased Cerebral Uptake of [18F]Fluoro-Deoxyglucose but not [1-14C]Glucose Early following Traumatic Brain Injury in Rats

“…Thus it cannot be excluded that changed expression of glucose transporters, shown to occur following diffuse brain injury and hypoxia-ischemia in the immature rat brain (Hamlin et al, 2001;Vannucci et al, 1998), influence transport of glucose and thus lCMR Glc calculations, at least at the 12-h post-injury time point. Previous studies demonstrated a changed l of the LC following both hypo-and hyperglycemia (Crane et al, 1983;Mori et al, 1989), and the LC was also changed following cerebral ischemia associated with a critically reduced cerebral blood flow (Greenberg et al, 1992;Nakai et al, 1987b). Finally, the release of lysosomal acid hydrolases after brain injury might alter the value of F by causing hydrolysis of 2-deoxyglucose 6-phosphate (Nakai et al, 1987a).…”

“…Early reports showed that the LC may change, at least regionally, during various physiological states of the brain, including hypoglycemia (Pardridge et al, 1982a(Pardridge et al, , 1982b. A changed LC was also observed following cerebral ischemia in cats, following ischemia and seizures in rats, and following human TBI, suggesting dynamic changes to the LC postinjury (Crane et al, 1983;Nakai et al, 1987b;Wu et al, 2004). The influence of FDG kinetics in direct comparison to other markers of glucose and energy metabolism has not yet been evaluated in experimental TBI.…”