After brain ischemia, dissimilar disturbances in morphology and energy metabolism have become evident in cortex and hippocampus the reason of which has not been completely elucidated as yet. Aged male Wistar rats underwent a 15 min complete cerebral ischemia induced by occlusion of the carotid and vetebral arteries and by hypovolemic hypotension. Thereafter, normotensive recirculation of the brain was established and the animals were allowed to recover for either 60 min, or 24 h, or 48 h, or 72 h, or 96 h. In cerebral cortex and hippocampus, the concentrations of glucose, lactate, and energy-rich compounds were measured by means of standard enzymatic methods. After ischemia, the ischemia induced metabolic abnormalities as measured as concentrations of glucose and lactate, and as energy-rich compounds normalized rapidly. After 48 and 72 h recirculation, a disturbance in glucose breakdown and an imbalance in energy metabolism became manifest in cerebral cortex, and even earlier (24 h) and longer (96 h), and more severe, in hippocampus. These changes may contribute to delayed neuronal damage and cell death in the areas studied. © 1988.
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