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To test the hypothesis that the sympathetic nervous system plays a role in cerebral blood flow regulation in patients with arteriovenous malformations (AVM).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.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).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.