Abstract
The pathophysiology of brain ischemia is characterized by a complex sequence of events, which include biochemical, hemodynamic and electrophysiological processes. Decreases in cerebral blood flow (CBF) below a critical threshold result in energy failure, tissue acidosis, disturbed ion homeostasis, with cellular Na+ and Ca++ influx and K+ efflux, membrane depolarization, and cytotoxic edema. There is a massive release of excitatory amino acid neurotransmitters (glutamate and aspartate) which triggers further membrane depolarization and an additional accumulation of intracellular Ca++. This accumulation of free cytosolic intracellular Ca++ appears to play a key role in the progression of events towards irreversible neuronal damage, in that it leads to an activation of a series of neurotoxic processes including lipid peroxidation, free radical generation, activation of proteolytic enzymes and pathological gene activation. The formation of vasogenic tissue edema is another important consequence of brain ischemia, which frequently complicates the clinical situation.
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© 1991 Springer Science+Business Media New York
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Phillis, J.W., Lin, Y. (1991). Oxypurinol Reduces Ischemic Brain Injury in the Gerbil and Rat. In: Harkness, R.A., Elion, G.B., Zöllner, N. (eds) Purine and Pyrimidine Metabolism in Man VII. Advances in Experimental Medicine and Biology, vol 309A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-2638-8_77
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DOI: https://doi.org/10.1007/978-1-4899-2638-8_77
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