Changes in glucose utilization in the rat brain after transient forebrain ischemia.

Abstract

Although several local cerebral glucose utilization (LCGU) studies using rat forebrain ischemia models have been performed to date, none that investigate long-term postischemic changes in LCGU throughout the brain have been reported. We investigated postischemic changes throughout the brain over 14 days using a rat forebrain ischemia model. Cerebral ischemia was produced using the rat four-vessel occlusion model. After 30 minutes of ischemia cerebral blood flow was restored, and LCGU in 34 structures in the brain was evaluated at 1, 3, 5, 7, and 14 days after ischemia. LCGU changes were characterized and could be divided into two major patterns, type 1 and type 2. In type 1, LCGU was reduced remarkably at 1 and 3 days, and it returned to near the control level at 5 days. In type 2, LCGU was reduced mildly at 1 day and returned to near the control level at 3 days. Included in type 1 were the severely ischemic structures such as the cerebral cortices and striatum. Included in type 2 were the less severely ischemic structures such as the midbrain, cerebellum, and pons and medulla oblongata. Drastic changes in LCGU took place not only in gray matter but also in white matter, and the patterns of LCGU changes were similar in both regions. Atypical changes in LCGU were observed in the hippocampal CA1 and substantia nigra pars reticulata. In both structures, LCGU was remarkably increased around 7 days after ischemia. There are two major patterns of LCGU changes after transient forebrain ischemia. LCGU changes in the hippocampal CA1 and substantia nigra pars reticulata are atypical.