Abstract— Energy metabolism was studied in the cerebral cortex of gerbils during and following ischemia induced by 1 h of unilateral carotid artery occlusion. An aneurysm clip was applied to the right common carotid artery of 50‐70 g gerbils under brief halothane anesthesia, and the clip was removed 1 h later. Clinical state (gait, responsiveness, seizures) was evaluated during carotid occlusion, and 40% of the animals showed clinical evidence of stroke. Cortical energy stores (2 ATP + ADP + P‐creatine) were more than half depleted in the ipsilateral cortex of clinically‐affected gerbils, and glucose fell by 75%; lactate rose over 7‐fold in the same specimens. After release of the carotid clip, clinical state improved, and biochemical abnormalities partially resolved. However, even after 24 h, the concentration of ATP and the total pool of adenine nucleotides remained subnormal. Metabolic activity in the ischemic cortex, assessed as the utilization of high‐energy phosphates following decapitation, was normal after 1 h of recovery and decreased (‐50%) after 24 h but was increased by more than 50% after 4 h. Cerebral glucose utilization, evaluated from autoradiographs prepared after intravenous administration of 2‐(1‐14C)deoxyglucose, was also increased in the cortex, hippocampus, and thalamus after 4 h of recovery. This post‐ischemic hypermetabolism in tissue damaged by ischemia may identify a critical period for cell repair, when therapy could be decisive.
Journal of Neurochemistry – Wiley
Published: Jan 1, 1977
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