Local cerebral glucose utilization in chronic middle cerebral artery occlusion in the cat

This study examines the correlation between local CMR(glc) (LCMR(glc)) alterations and clinicopathological changes in a chronic middle cerebral artery (MCA) occlusion model in the cat. The left MCA was occluded for a period of 2 h. The animals were grouped into mild, moderate, and severe ischemia based on the depression of the EEG 30 min after the MCA occlusion. Following release of the clip, the animals were allowed to recover for a week during which time daily neurological examinations were performed. On the seventh day [¹⁴C]2-deoxyglucose was injected for the determination of LCMR(glc). Alternative blocks were processed for histological evaluation in which both neuronal and phagocytic changes were graded into four categories (0 = normal to 3 = severe). LCMR(glc) μmol/100 g/min) in the ischemic hemisphere (all histological grades) was significantly lower than the metabolic rate in comparable regions of the sham MCA occlusion group. Regions with significant phagocytosis (grade 2 and 3) invariably exhibited activated glucose metabolism (57.4 ± 8.5 and 105.9 ± 6.8 μmol/100 g/min, respectively), which was significantly higher than in regions without phagocytosis (30.4 ± 0.8 μmol/100 g/min). There was a significant gradient of metabolism in the central, peripheral, and boundary zone and the non-MCA territory in the animals with severe ischemic lesions. LCMR(glc) in the central MCA territory was well correlated with the EEG amplitude changes (r = 0.82, p < 0.05) and the morphological score (r = -0.89, p < 0.05). The metabolic rate was significantly depressed in both the ipsilateral and the contralateral central MCA territories in comparison with the sham occlusion animals. The depression in LCMR(glc) in the contralateral hemisphere correlated well with the concomitant depression in the contralateral EEG amplitude. These studies demonstrate that local heterogeneous metabolic alterations and contralateral cortical diaschisis exist chronically following temporary MCA occlusion and that the increases in local cerebral glucose metabolism seen in chronic stroke may be due to phagocytotic activity.