Background: In a situation with normal cerebral blood flow (CBF) and without increased energy utilization, increased glucose utilization (CGU) can be a sign of impaired mitochondrial metabolism, which may be an early step in the neurodamaging cascade during reperfusion after hypoxia-ischemia(HI).

Subjects: 7-day-old rats underwent unilateral carotid artery ligation and 70 min of HI.

Measurements: At 3, 6, 12, 24, and 48 or 72 h after the insult the rCGU was measured by the 2-deoxyglucose method, and CBF by the iodoantipyrine method. These were compared to hematoxylin-eosine staining and microtubule associated protein 2 (MAP 2) immunostaining in adjacent sections.

Results: There was an ipsilateral regional increase of CGU compared to the contralateral hemisphere 3-6 h after HI in areas with partioal MAP2 loss, while at 12 h central hypo-glucose utilizing areas, with total loss of MAP2, were surrounded by only a rim of tissue with increased CGU. At 24 and 72 h after the insult, no regions with increased CGU remained. Despite loss of MAP2 immunostaining the cortical CBF was not reduced until 48 h after HI, while the CBF in the caudate-putamen was decreased compared to the contralateral side already at 3 h after HI.

Conclusions: The progression from increased to decreased CGU during 24 h after HI, indicates that areas with increased CGU, indicating mitochondrial impairment, are at risk of developing irreversible tissue necrosis.