Abstract
Injury to the brain by trauma, ischemia or other causes may lead to formation of focal tissue necrosis and opening of the blood-brain barrier resulting in secondary brain damage, as e.g. vasogenic edema. A variety of chemical mediators, which are liberated or activated in the focus, have been associated with the development of secondary processes. Currently, our laboratory is studying among others the kallikrein-kinin-system (KK-System) [1, 2, 3, 5, 7, 8]. Previous investigations have shown that ventriculo-cisternal perfusion with plasma or with the active principle bradykinin results in brain edema [2, 3, 7, 8]. Now, we report on recently conducted experiments where an activation of the kallikrein-kinin-system was studied in vasogenic edema induced by focal brain trauma.
Supported by Deutsche Forschungsgemeinschaft, Ba 452/5
The excellent technical and secretarial assistance of Ulrike Goerke, Angelika Müller, Sylvia Schneider, Isolde Moll, Mechthild Stein, and Christa Chaudhry is gratefully acknowledged
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References
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Dedicated to Prof. Dr. med. Dr. h. c. Walter Brendel on the occasion of his 60th birthday
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© 1982 Springer-Verlag Berlin Heidelberg
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Maier-Hauff, K. et al. (1982). The Kallikrein-Kinin-System as Mediator in Cerebral Edema, Recent Progress. In: Hartmann, A., Brock, M. (eds) Treatment of Cerebral Edema. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-68707-5_5
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DOI: https://doi.org/10.1007/978-3-642-68707-5_5
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-11751-3
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