Objective: In an animal model, we tested the hypothesis that intracerebral, extracellular norepinephrine (NE) influences cerebral blood flow (CBF) in the presence of cerebral arteriovenous malformations (AVMs).
Methods: A microdialysis (MD) probe was implanted into the cortices of Sprague-Dawley rats 3 months after the creation of extracranial arteriovenous fistulae (AVFs; n = 19), carotid ligation (n = 10), and cervical vessel preparation (sham operations; n = 8). Ipsilateral regional cortical oxygen saturation (microspectrophotometry) and regional cerebral blood flow (laser Doppler flowmetry) were scanned with simultaneous MD sampling for NE (high-performance liquid chromatography). Local CBF and cortical capillary oxygen saturation (SO2) were recorded continuously with serial MD sampling after fistula occlusion for 100 minutes. The scanning protocol was repeated after 120 minutes. Values were compared by analysis of variance and Duncan's test (P < 0.05; values expressed as mean +/- standard deviation).
Results: NE was highest in sham-operated animals and lowest after carotid ligation as compared with before and after the creation of the AVFs (sham operations, 5.9 +/- 2.3 nmol/L; common carotid artery ligation, 2.4 +/- 1 nmol/L; before creation of AVF, 4.1 +/- 1.9 nmol/L; after creation of AVF, 4.1 +/- 2.3 nmol/L). Regional cortical oxygen saturation differed significantly between all groups; regional cerebral blood flow was lower only in sham-operated animals (sham operations, 210 +/- 75 laser Doppler units [LDU], 71 +/- 13% SO2; common carotid artery ligation, 250 +/- 82 LDU, 62 +/- 19% SO2; before creation of AVF, 249 +/- 96 LDU, 65 +/- 14% SO2; after creation of AVF, 256 +/- 82 LDU, 74 +/- 10% SO2). After fistula occlusion, a sustained CBF increase for 100 minutes up to 40% above baseline (i.e., regional cerebral blood flow and regional cortical oxygen saturation before occlusion) was observed. SO2 increased to 16% after 120 minutes. Peaks of NE concentrations occurred 40 minutes and 100 minutes after fistula occlusion.
Conclusion: The model seems to be valid for the simulation of events that occur before and after the obliteration of human cerebral AVMs in most cases, but not in those prone to hyperperfusion syndromes. The results provide evidence that cerebral sympathetic nervous system activity can be monitored by in vivo MD and that NE may play a role in CBF control before and after the obliteration of AVFs.