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Cerebral Ischemia and Polyphosphoinositide Metabolism

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Part of the book series: Advances in Neurochemistry ((ANCH,volume 7))

Abstract

Cerebral ischemia due to cerebrovascular occlusion is one of the most devastating diseases confronting mankind. The brain is critically dependent on a balanced supply of oxygen and glucose from blood, and cessation of blood flow even for a short time may result in severe neuronal damages and eventually neuronal cell death. In many ways, the initial phase of ischemic insult is like an acute neuronal stimulation which is accompanied by synaptic membrane depolarization, calcium influx and neurotransmitter release (see the review by Nemoto [1985]). However, unlike electroconvulsive shock or drug-induced seizures, neuronal events associated with ischemia are further complicated by cellular deprivation of glucose and high-energy metabolites, and this, in turn, may lead to an increase in the levels of lactate and other metabolic end products (Lowry et al., 1964; Kobayashi et al., 1977; Levy and Duffy, 1977,1985; Nowak et al., 1985). There are also changes in membrane phospholipids as a result of the ischemic insult; some of these have been described previously (Sun, 1988).

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© 1992 Springer Science+Business Media New York

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Sun, G.Y. (1992). Cerebral Ischemia and Polyphosphoinositide Metabolism. In: Bazan, N.G., Braquet, P., Ginsberg, M.D. (eds) Neurochemical Correlates of Cerebral Ischemia. Advances in Neurochemistry, vol 7. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3312-2_11

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  • DOI: https://doi.org/10.1007/978-1-4615-3312-2_11

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