Source:http://linkedlifedata.com/resource/pubmed/id/11370243
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2001-5-23
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pubmed:abstractText |
The effect of 'chemical sympathectomy', produced by daily intraperitoneal injections of guanethidine sulphate for six weeks, was studied in sedentary rats and in rats chronically exercised by swimming. The guanethidine-treatment itself caused the following changes. There was a reduction in the rate of weight gain resulting in a 7% lower final body weight. Organ content of noradrenaline was decreased by 90% in spleen and submandibular glands and by 83% in the heart. Urinary excretion of noradrenaline was also decreased, but to a lesser degree, both during rest (45% lower) and after acute exercise (46% lower), while the urinary excretion of adrenaline was no different from that of controls. There was a compensatory adrenal hypertrophy in the guanethidine-treated rats, with a significant increase in adrenal catecholamine levels that was more pronounced for noradrenaline (+45%) than for adrenaline (+11%). Chronic physical exercise produced the expected degree of cardiac hypertrophy in untreated rats, but this adaptive cardiac hypertrophy was completely absent in the exercised guanethidine-treated rats. The results indicate, firstly that a good degree of chemical sympathectomy was obtained and that the persistence of a considerable urinary excretion of catecholamines in the guanethidine-treated rats was due to a compensatory increase in the secretory activity of the adrenal medulla. Secondly, it is suggested that the adaptive cardiac hypertrophy produced by chronic exercise is not caused by a direct effect of the increased work load on the cardiac muscle cell, but is instead mediated by release of a trophic factor from cardiac sympathetic nerves, probably noradrenaline itself but possibly a secretory protein.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0306-4522
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
497-507
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11370243-Adrenal Medulla,
pubmed-meshheading:11370243-Animals,
pubmed-meshheading:11370243-Body Weight,
pubmed-meshheading:11370243-Catecholamines,
pubmed-meshheading:11370243-Guanethidine,
pubmed-meshheading:11370243-Heart,
pubmed-meshheading:11370243-Hypertrophy,
pubmed-meshheading:11370243-Male,
pubmed-meshheading:11370243-Myocardium,
pubmed-meshheading:11370243-Organ Size,
pubmed-meshheading:11370243-Physical Conditioning, Animal,
pubmed-meshheading:11370243-Rats,
pubmed-meshheading:11370243-Rats, Sprague-Dawley,
pubmed-meshheading:11370243-Sympathectomy, Chemical,
pubmed-meshheading:11370243-Sympathetic Fibers, Postganglionic,
pubmed-meshheading:11370243-Sympatholytics
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pubmed:year |
1976
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pubmed:articleTitle |
Prevention of exercise-induced cardiac hypertrophy in rats by chemical sympathectomy (guanethidine treatment).
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pubmed:affiliation |
Department of Physiology I, Karolinska Institute, S-104 01 Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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