Abstract
Formation of vasogenic brain edema is facilitated by arteri-olar dilation and venular constriction as well as an increase of vascular permeability. A previous study has shown that the cerebral water content is increased after ventriculo-cisternal perfusion with bradykinin5. In addition, uptake of plasma kininogen has been demonstrated in damaged brain1. Therefore, bradykinin may be involved in the formation and spreading of brain edema. Since only few and contradictory reports on the vasomotor effect of bradykinin on isolated cerebral arteries are available3,2 the aim of the present study was to test the vasomotor effect of bradykinin on cerebral vessels in vivo.
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© 1984 Plenum Press, New York
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Wahl, M., Unterberg, A., Baethmann, A. (1984). Vasoactive Effects of Bradykinin on Cerebral Vessels and its Possible Role as a Mediator of Vasogenic Brain Edema. In: Go, K.G., Baethmann, A. (eds) Recent Progress in the Study and Therapy of Brain Edema. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4616-6_23
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DOI: https://doi.org/10.1007/978-1-4684-4616-6_23
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