Linked Life Data

10988269

Source:http://linkedlifedata.com/resource/pubmed/id/10988269

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-10-2
pubmed:abstractText
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.
pubmed:grant
pubmed:keyword
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
383-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10988269-Adult, pubmed-meshheading:10988269-Analysis of Variance, pubmed-meshheading:10988269-Baroreflex, pubmed-meshheading:10988269-Blood Flow Velocity, pubmed-meshheading:10988269-Blood Pressure, pubmed-meshheading:10988269-Carbon Dioxide, pubmed-meshheading:10988269-Cerebrovascular Circulation, pubmed-meshheading:10988269-Ganglionic Blockers, pubmed-meshheading:10988269-Humans, pubmed-meshheading:10988269-Hyperventilation, pubmed-meshheading:10988269-Hypocapnia, pubmed-meshheading:10988269-Phenylephrine, pubmed-meshheading:10988269-Supine Position, pubmed-meshheading:10988269-Sympathetic Nervous System, pubmed-meshheading:10988269-Tilt-Table Test, pubmed-meshheading:10988269-Trimethaphan, pubmed-meshheading:10988269-Ultrasonography, Doppler, Transcranial, pubmed-meshheading:10988269-Vascular Resistance, pubmed-meshheading:10988269-Vasoconstriction, pubmed-meshheading:10988269-Vasoconstrictor Agents
pubmed:year
2000
pubmed:articleTitle
Interaction of carbon dioxide and sympathetic nervous system activity in the regulation of cerebral perfusion in humans.
pubmed:affiliation
Clinical Research Center, Franz-Volhard Clinic, Humboldt University, Berlin, Germany. jordan@fvk-berlin.de
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.