TEMPORAL CHANGES OF REGIONAL GLUCOSE USE, BLOOD-FLOW, AND MICROTUBULE-ASSOCIATED PROTEIN-2 IMMUNOSTAINING AFTER HYPOXIA-ISCHEMIA IN THE IMMATURE RAT-BRAIN
E. Gilland et al., TEMPORAL CHANGES OF REGIONAL GLUCOSE USE, BLOOD-FLOW, AND MICROTUBULE-ASSOCIATED PROTEIN-2 IMMUNOSTAINING AFTER HYPOXIA-ISCHEMIA IN THE IMMATURE RAT-BRAIN, Journal of cerebral blood flow and metabolism, 18(2), 1998, pp. 222-228
In a situation with normal CBF and without increased energy utilizatio
n, increased glucose utilization (CMRglc) can be a sign of impaired mi
tochondrial metabolism, which may be an early step in the injury casca
de during reperfusion after hypoxia-ischemia (Hl). Seven-day-old rats
underwent unilateral carotid artery ligation and 70 minutes of HI. At
3, 6, 12, 24, and 48 or 72 hours after the insult, the CMRglc was meas
ured by the 2-deoxyglucose method, and CBF by the iodoantipyrine metho
d. These were compared with hematoxylin-eosin staining and microtubule
-associated protein 2 (MAP 2) immunostaining in adjacent sections. In
the ipsilateral hemisphere, there appeared regions with increased CMRg
lc compared with the contralateral hemisphere 3 to 12 hours after Hl t
hat also showed partial loss of MAP 2 immunostaining and early ischemi
c changes. These areas receded, leaving central glucose hypo-utilizing
areas with complete loss of MAP 2 immunostaining and histologic infar
ction, surrounded by only a rim of tissue with increased CMRglc. At 24
and 72 hours after the insult, no regions with increased CMRglc remai
ned. Despite loss of MA 2 immunostaining and histologic signs of infar
ction at 24 hours, cortical CBF was not reduced until 48 hours after H
I, whereas the CBF in the caudate-putamen already was decreased compar
ed with the contralateral side at 3 hours after HI. In conclusion, ear
ly reperfusion is characterized by glucose hyperutilizing areas in the
cerebral fortes, followed by a secondary phase with low CMRglc and in
farction.