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.
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Gilland, E., Bona, E. & Hagberg, H. Temporal changes of regional glucose use, blood flow and MAP2 immunostaining after hypoxia-ischemia in the immature rat brain 15. Pediatr Res 42, 387 (1997). https://doi.org/10.1203/00006450-199709000-00035
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DOI: https://doi.org/10.1203/00006450-199709000-00035