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Glutamate And Free Fatty Acid Concentrations In Extracellular Vasogenic Edema Fluid

K. Hauff, M. Lange, L. Schürer, C. Guggenbichler, W. Vogt, K. Jacob, A. Baethmann
Published 1984 · Chemistry

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Traumatic or ischemic injury to the brain causes focal tissue necrosis together with an opening of the blood-brain barrier leading to an influx of vasogenic edema into the cerebral parenchyma. Clinical and experimental observations suggest an involvement of chemical factors, or compounds mediating secondary brain damage, such as vasogenic brain edema. Mediators may enhance the primary damage inflicted to the blood brain barrier, induce derangements of the cerebral microcirculation, and cause formation of secondary cytotoxic necrosis, or cell swelling in focal and perifocal areas. Many systems and compounds have been studied in this context2. A great number of reports, including those of ourselves demonstrate glutamate and free fatty acids to exhibit powerful neurotoxic properties. These findings together with the occurrence of glutamate and free fatty acids either in the intra-cellular compartment, or the lipid moiety in vast amounts in normal brain render both substances excellent candidates as mediators of secondary brain damage. Exposure of brain tissue to glutamate by iontophoretic administration to cerebral cortex, or by ventriculo-cisternal perfusion in-vivo was found to induce swelling and destruction of cellular elements, or gross brain edema, respective-ly14,l,9,13.



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