title: Norepinephrine and cerebral blood flow regulation in patients with arteriovenous malformations.
abstract: OBJECTIVE
  To test the hypothesis that the sympathetic nervous system plays a role in cerebral blood flow regulation in patients with arteriovenous malformations (AVM).
  
  
  METHODS
  Cortical interstitial norepinephrine was measured by means of microdialysis, regional cerebral blood flow was measured by a thermal diffusion technique, and regional oxygen saturation (SO2) was measured by microspectrophotometry in 12 patients harboring cerebral AVMs (AVM group) and in 15 patients with deep-seated nonvascular lesions (control group) before and after resection. Measurements were compared according to groups and times of measurements. All values are given as means +/- standard deviation.
  
  
  RESULTS
  Cortical regional SO2 increased significantly (P < 0.05) in both groups after surgery (AVM group: presurgery 52.4 +/- 12.5% SO2, postsurgery 71.4 +/- 7.4% SO2; control group: presurgery 57.1 +/- 8.4% SO2, postsurgery 69.9 +/- 8.7% SO2), whereas regional cerebral blood flow increased only in the AVM group (AVM group: presurgery 18.9 +/- 6.6 ml/100 g/min, postsurgery 26.2 +/- 6.9 ml/100 g/min; control group: presurgery 20.1 +/- 7.6 ml/100 g/min, postsurgery 19.4 +/- 7.8 ml/100 g/min). Norepinephrine concentrations were significantly lower in the AVM group as compared with the control group before surgery. Although there was no significant difference between pre- and postsurgery conditions in the AVM group, the norepinephrine level of the control group was significantly lower after surgery (AVM group: presurgery 3.3 +/- 1.2 nmol/L, postsurgery 2.9 +/- 1.7 nmol/L; control group: presurgery 5.4 +/- 1.4 nmol/L, postsurgery 4.2 +/- 1.1 nmol/L).
  
  
  CONCLUSIONS
  Chronically lowered perfusion pressure seems to induce the hypothesized adaptive down-regulation of sympathetic nervous system activity, yet protective up-regulation after a sudden elevation of cerebral perfusion pressure after AVM excision could not be shown in this study.
authors.affiliation: Department of Neurosurgery, Technical University of Munich, Munich, Germany.
authors.forename: Carsten
authors.initials: C
authors.lastname: Stüer
authors.forename: Toshiki
authors.initials: T
authors.lastname: Ikeda
authors.forename: Michael
authors.initials: M
authors.lastname: Stoffel
authors.forename: Gerd
authors.initials: G
authors.lastname: Luippold
authors.forename: Oliver
authors.initials: O
authors.lastname: Sakowitz
authors.forename: Karl
authors.initials: K
authors.lastname: Schaller
authors.forename: Bernhard
authors.initials: B
authors.lastname: Meyer
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000378:metabolism* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D015331:Cohort Studies; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D002538:Intracranial Arteriovenous Malformations / Q000378:metabolism* / Q000503:physiopathology* / Q000601:surgery; D007427:Intracranial Pressure / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology
chemical_list: D009638:Norepinephrine