Linked Life Data

2455164

Source:http://linkedlifedata.com/resource/pubmed/id/2455164

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1988-7-29
pubmed:abstractText
Metabolism of catecholamines was monitored by in vivo voltammetry in the ventrolateral medulla (encompassing the A1 group of noradrenergic cell bodies) of anesthetized rats and in the locus coeruleus of behaving rats. Activation of metabolism of catecholamines was produced by using: (1) controlled hypotension (sodium nitroprusside, mean arterial pressure reduced to approximately 60 mm Hg for 60 min, n = 5) in anesthetized animals; and (2) immobilization (10 min) of conscious rats (n = 5). Clonidine, 200 micrograms/kg (i.p., n = 3), suppressed almost entirely the activation of the metabolism of catecholamines secondary to controlled hypotension in the ventrolateral medulla. Clonidine, 50 (n = 3) to 200 (n = 5) micrograms/kg (i.p.), produced a dose-dependent suppression of the activation of the metabolism of catecholamines induced by immobilization in the locus coeruleus of conscious rats. The results obtained from this study provide a biochemical rationale for the use of alpha 2-agonists in conditions where central or peripheral noradrenergic activity is heightened.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
10 Suppl 12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S128-34
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
The ability of the alpha 2-adrenergic agonist clonidine to suppress central noradrenergic hyperactivity secondary to hemodynamic or environmental stimuli.
pubmed:affiliation
Neuropharmacology, A. Carrel School of Medicine, Lyon, France.
pubmed:publicationType
Journal Article