Summary
Exposure of rat brain to glutamate or homologous plasma by ventriculocisternal perfusion leads to cerebral edema. After glutamate perfusion, brain edema takes 24 h to develop, while edema is present immediately after perfusion with undiluted plasma. The increase in cerebral water content produced by ventricular perfusion with glutamate or plasma is relatively small, but nevertheless significant. After glutamate perfusion, the K+ content of the brain is reduced, while it remains unchanged after perfusion with plasma. The kininogen concentration of the plasma perfusate leaving the ventricles is significantly reduced suggesting a release of kinins during perfusion. The blood-brain barrier permeability to Evans blue was not enhanced after either perfusion with glutamate or plasma. The data raise the possibility that glutamate as well as the kininogen-kinin system play a role as brain edema factors.
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References
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© 1976 Springer-Verlag Berlin · Heidelberg
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Oettinger, W., Baethmann, A., Rothenfusser, W., Geiger, R., Mann, K. (1976). Tissue and Plasma Factors in Cerebral Edema. In: Pappius, H.M., Feindel, W. (eds) Dynamics of Brain Edema. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66524-0_27
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DOI: https://doi.org/10.1007/978-3-642-66524-0_27
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-08009-1
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