gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Bradykinin in blood and CSF after cerebral lesions – correlation with ICP, brain edema and clinical outcome

Bradykininbestimmung im Serum und Liquor nach zerebralen Läsionen – Korrelation mit dem ICP, Hirnödem und Outcome

Meeting Abstract

  • corresponding author M. Kunz - Neurochirurgische Klinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München
  • J. Nussberger - Service d’Angiologie CHUV Lausanne
  • M. Holtmannspötter - Abteilung für Neuroradiologie, Klinikum Großhadern, Ludwig-Maximilians-Universität München
  • N. Plesnila - Neurochirurgische Klinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München
  • S. Zausinger - Neurochirurgische Klinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocFR.07.08

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2007/07dgnc111.shtml

Published: April 11, 2007

© 2007 Kunz et al.
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Outline

Text

Objective: The nonapeptide Bradykinin (Bk) was shown to stimulate the production of cytokines, NO, free radicals and excitatory amino acids, producing cytotoxity, vasodilation, blood brain barrier disruption and therefore enhancing brain edema. Purpose of this prospective study was to measure Bk concentrations time dependently in CSF and blood of patients with traumatic brain injury (TBI), subarachnoid or intracerebral hemorrhage and cerebral ischemia and to correlate concentrations with ICP, extent of edema and clinical outcome.

Methods: 18 patients (mean age:49.3y) suffering from acute cerebral lesions (5 with traumatic brain injury, 8 with subarachnoid and 3 with intracerebral hemorrhage, 2 with ischemic stroke) and 3 patients with myelograms as controls, were enrolled. Bk samples in CSF and blood were collected after the insult and during the following up to 9 days. ICP, clinical score (GCS) and extent of the lesion and of cerebral edema (6-point scale) at sampling time point as well as clinical score at discharge (GOS) were assessed and correlated with Bk concentrations. Liquid phase extraction, high performance liquid chromatography and RIA were used for measurement of Bk concentrations.

Results: While serum Bk levels (fmol/ml) were within normal limits in all patients (1.2-1.9), a tendency towards increased CSF Bk levels was observed in patients with large infarction (3.0±2.8), intracerebral (2.2±1.2) and subarachnoid (1.6±1.4) hemorrhage and after TBI (1.8±1.3) compared to controls (1.2±0.8). CSF Bk levels did not vary significantly between the different pathologies and no significant correlation with GCS was found during the observation period. However, CSF Bk levels correlated significantly with ICP values in patients with intracerebral (r=0.8, p=0.02) and subarachnoid (r=0.5, p=0.03) hemorrhage and with TBI patients (r=0.6, p=0.02). Furthermore, in patients with subarachnoid and intracerebral hemorrhage, CSF Bk levels correlated significantly with the extent of edema in CT (r=0.5, p=0.04 and r=0.7, p=0.09) and with GOS (r=0.7, p=0.04 and r=0.7, p=0.01).

Conclusions: Our results demonstrate that acute cerebral lesions are associated with an activation of the kallikrein-kinin system with increased Bk levels in the CSF. Especially after subarachnoid and intracerebral bleeding, CSF Bk concentrations correlate with ICP, extent of edema evolution and with GOS at discharge. Further studies with larger group sizes and Bk sampling at very early time points after the insult might provide fundamental information for potential therapeutic studies, e.g. investigating the effects of Bk receptor antagonists.