Abstract
Evidence of a role of the kallikrein-kinin (KK) system as mediator in vasogenic brain edema is impressive, albeit not complete [1]. Experimental findings demonstrate that kinins, the active peptides of the KK system, induce brain edema of gray and white matter [10]. Cerebral administration of kinins opens the blood-brain barrier for small molecules, which may be viewed as a mechanism leading to interstitial fluid accumulation [11, 12]. Moreover, experimental injury to the brain (cold lesion) is associated with the formation of kinins in and around the primary insult [6]. However, no evidence is available so far to indicate whether specific inhibition of the release or function of kinins is therapeutically beneficial in brain edema.
The work described in this paper was supported by grant no. Ba 452/6-5 from the Deutsche Forschungsgemeinschaft
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Unterberg, A., Dautermann, C., Müller-Esterl, W., Baethmann, A. (1985). Inhibition of the Kallikrein-Kinin System in Vasogenic Brain Edema. In: Inaba, Y., Klatzo, I., Spatz, M. (eds) Brain Edema. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70696-7_45
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DOI: https://doi.org/10.1007/978-3-642-70696-7_45
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