Blood Flow, Metabolism, and Function of the Brain During Cerebral Administration of Bradykinin

  • A. Unterberg
  • U. Hack
  • A. Baethmann
Part of the Advances in Neurosurgery book series (NEURO, volume 13)


The kallikrein-kinin system is considered a mediator of secondary brain damage, e.g., evolving from traumatic lesions or cerebral ischemia (1). The kinin peptides are powerful dilatory substances of the peripheral vasculature and they increase its permeability (3, 6). Activation of the system and release of kinins occur in tissue injury associated with coagulation and inflammation (3, 6). Evidence of pathophysiological effects in the CNS induced by kinins has been provided. Superfusion of cerebral cortex with bradykinin opens the blood-brain barrier to small molecules and dilates cerebral arteries (8, 10). Moreover, ventricle perfusion with bradykinin was found to cause cerebral edema, and focal injury of the brain to result in cerebral uptake of plasma kininogens and formation of kinins (5, 7).


Cerebral Blood Flow Secondary Brain Damage Vasogenic Brain Edema Cerebral Uptake Cerebral Electrical Activity 
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Copyright information

© Springer-Verlag Berlin Heidelberg 1985

Authors and Affiliations

  • A. Unterberg
    • 1
  • U. Hack
    • 1
  • A. Baethmann
    • 1
  1. 1.Institut für Chirurgische Forschung, Klinikum GroßhadernUniversität MünchenMünchen 70Germany

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