title: Interaction of carbon dioxide and sympathetic nervous system activity in the regulation of cerebral perfusion in humans.
abstract: Recent studies suggest that activation of the sympathetic nervous system either directly or indirectly influences cerebrovascular tone in humans even within the autoregulatory range. In 6 healthy subjects (aged 29+/-4 years), we used transcranial Doppler sonography to determine cerebral blood flow velocity during sympathetic activation elicited through head-up tilt (HUT) and sympathetic deactivation through ganglionic blockade. PaCO(2) was manipulated through hyperventilation and CO(2) breathing (5%). With subjects in the supine position and during HUT, mean arterial pressure was not influenced by PaCO(2). During ganglionic blockade, mean arterial pressure decreased markedly with hyperventilation (-13+/-1.9 mm Hg). Manipulation of sympathetic tone elicited only mild changes in cerebral blood flow (64+/-5.8 cm/s supine, 58+/-4.9 cm/s upright, and 66+/-6.2 cm/s during ganglionic blockade; P:=0.07 by ANOVA). The slope of the regression between PaCO(2) and mean velocity was 1.6+/-0.18 cm/(s. mm Hg) supine, 1.3+/-0.14 cm/(s. mm Hg) during HUT, and 2.3+/-0.36 cm/(s. mm Hg) during ganglionic blockade (P:<0.05). Spontaneous PaCO(2) and ventilatory response to hypercapnia were also modulated by the level of sympathetic activity. Changes in sympathetic tone have a limited effect on cerebral blood flow at normal PaCO(2) levels. However, the sympathetic nervous system seems to attenuate the CO(2)-induced increase in cerebral blood flow. This phenomenon may indicate a moderate direct effect of the sympathetic nervous system on the cerebral vasculature. Furthermore, sympathetic activation tends to increase ventilation and thus can indirectly increase cerebrovascular tone.
authors.affiliation: Clinical Research Center, Franz-Volhard Clinic, Humboldt University, Berlin, Germany. jordan@fvk-berlin.de
authors.forename: J
authors.initials: J
authors.lastname: Jordan
authors.forename: J R
authors.initials: JR
authors.lastname: Shannon
authors.forename: A
authors.initials: A
authors.lastname: Diedrich
authors.forename: B
authors.initials: B
authors.lastname: Black
authors.forename: F
authors.initials: F
authors.lastname: Costa
authors.forename: D
authors.initials: D
authors.lastname: Robertson
authors.forename: I
authors.initials: I
authors.lastname: Biaggioni
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D017704:Baroreflex / Q000502:physiology; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002245:Carbon Dioxide / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D005730:Ganglionic Blockers / Q000494:pharmacology; D006801:Humans; D006985:Hyperventilation / Q000503:physiopathology; D016857:Hypocapnia / Q000503:physiopathology*; D010656:Phenylephrine / Q000494:pharmacology; D016683:Supine Position / Q000502:physiology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D018667:Tilt-Table Test; D014294:Trimethaphan / Q000494:pharmacology; D017585:Ultrasonography, Doppler, Transcranial; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D005730:Ganglionic Blockers; D014662:Vasoconstrictor Agents; D002245:Carbon Dioxide; D010656:Phenylephrine; D014294:Trimethaphan