Titlebook: Clinical Pharmacology of Cerebral Ischemia; Gert J. Horst,Jakob Korf Book 1997 Springer Science+Business Media New York 1997 brain.brain i

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Anand Prasad Mishra,Soumyabrata Mondal5% of cardiac output. The amounts of energy metabolites (glucose and glycogen) and oxygen stored in the brain are so small that cessation of blood supply for only a few minutes leads to severe CNS damage. This vulnerability of the CNS mainly derives from the vulnerability of neurons, the major compo

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Imaging of Stroke,ographic technologies. Today, computer tomography (CT) and magnetic resonance imaging (MRI) are widely available .. CT is mainly used to distinguish between hemorrhagic and nonhemorrhagic pathology in the acute phase of stroke .. Both MRI and CT visualize morphological changes in the brain; MRI, how

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Glutamate Neurotoxicity and Stroke,many cortical efferent systems and in intrahippocampal pathways. When glutamatergic terminals are depolarized, vesicular glutamate is released into the synaptic cleft in a Ca.-dependent manner .. There, glutamate interacts with several distinct families of receptors located principally on postsynapt

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Free Radical-Mediated Cerebral Damage After Hypoxia/Ischemia and Stroke,d by energy transfer reactions in all life forms using oxygen. Under physiological conditions, sophisticated antioxidant defense systems prevent the reactive O. metabolites from potential injurious interactions with cell components critical for the viability of cells. However, under the conditions o

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Genomic Responses Following Cerebral Ischemia,rboxylase were induced in the cortex, despite an inhibition of the overall rate of protein synthesis . that persists for prolonged periods after the ischemic insult .. About 10 yr later, the postischemic synthesis of the heat shock protein HSP70, and glial fibrillary acidic protein (GFAP) was report

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