Uncoupling of local cerebral glucose metabolism and blood flow after acute fluid-percussion injury in rats

We assessed local cerebral glucose metabolism (lCMR(Glc)) and blood flow (ICBF) interrelationships in the first hour after parasagittal fluid-percussion head injury (FPI) in rats. Matched series were studied autoradiographically for lCMR(Glc) and lCBF with 2-[C-14]deoxyglucose and C-14-labeled iodoantipyrine, respectively. Three-dimensional autoradiographic-image mapping was used to generate average data sets from which a mean lCMR(Glc)-to-lCBF ratio data set was derived. lCBF in neocortical regions ipsilateral to the trauma were depressed, on average, by 44% compared with sham-FPI rats, whereas contralateral lCBF values were not altered. By contrast, lCMR(Glc) was elevated in many cortical and subcortical sites of both hemispheres; this amounted to 1.3- to 1.4-fold increases in neocortical regions in the thalamus and 1.6- to 1.7-fold increases in the hippocampus. The lCMR(Glc)-to-lCBF ratio data revealed striking elevations both ipsilateral (P = 7 x 10(-7)) and contralateral to the FPI (P = 0.003). The extent of metabolism-flow uncoupling, on average, amounted to 2.5-fold in the ipsilateral hippocampus and neocortex and 1.7-fold contralaterally. The loci of pronounced metabolism-flow dissociation corresponded closely to the previously documented histological distribution of neuronal necrosis. Our findings resemble events occurring in the acute focal ischemic penumbra and suggest that similar injury mechanisms may be operative.