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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1991-12-23
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pubmed:abstractText |
Vasomotor reactivity was assessed in vitro in arterial segments obtained from rabbits with different stages of atherosclerosis. Rabbits were fed a standard chow diet (controls) or a cholesterol-enriched diet to induce hypercholesterolemia and atherosclerosis. A third group received the hydroxymethylglutaryl coenzyme A reductase inhibitor, lovastatin, simultaneously with the cholesterol diet. Contractile responses of thoracic aortas to norepinephrine, serotonin, and potassium-rich solution, as well as endothelium-dependent dilations to acetylcholine, were compared after 2 and 4 months on the respective diet. Additionally, plasma cholesterol levels and the amount of plaques covering the intimal surface (as a percentage of the intimal surface) were determined; transmission electron microscopy of atherosclerotic arteries was also performed. After 2 months, the only difference was an enhancement of contractile responses to serotonin in the cholesterol-fed versus the control group. After 4 months on the diet, contractile responses to serotonin were further enhanced, and norepinephrine- and potassium-induced vasoconstrictions were now also significantly enhanced in cholesterol-fed animals versus controls. Endothelium-dependent vasodilations were simultaneously reduced in cholesterol-fed animals. These alterations were partly prevented in cholesterol-fed and lovastatin-treated animals. Suppression of nitric oxide synthesis in control aortas by NG-nitro-L-arginine did not reveal any significant increases in contractile responses. Contractile responses to serotonin were enhanced after 2 months on the diet but before the appearance of intimal plaques, whereas attenuation of endothelium-dependent dilations, as well as the further enhancement of contractile responses to serotonin and to other agonists, were closely correlated with the degree of intimal plaques after 4 months on the diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Arginine,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol,
http://linkedlifedata.com/resource/pubmed/chemical/Lovastatin,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroarginine,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents
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pubmed:status |
MEDLINE
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pubmed:issn |
1049-8834
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
11
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1712-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1931872-Animal Feed,
pubmed-meshheading:1931872-Animals,
pubmed-meshheading:1931872-Aorta, Thoracic,
pubmed-meshheading:1931872-Arginine,
pubmed-meshheading:1931872-Arteriosclerosis,
pubmed-meshheading:1931872-Cholesterol,
pubmed-meshheading:1931872-Endothelium, Vascular,
pubmed-meshheading:1931872-Hypercholesterolemia,
pubmed-meshheading:1931872-Lovastatin,
pubmed-meshheading:1931872-Nitroarginine,
pubmed-meshheading:1931872-Rabbits,
pubmed-meshheading:1931872-Vasoconstriction,
pubmed-meshheading:1931872-Vasoconstrictor Agents,
pubmed-meshheading:1931872-Vasodilation
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pubmed:articleTitle |
Hypercholesterolemia and atherosclerosis change vascular reactivity in rabbits by different mechanisms.
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pubmed:affiliation |
Department of Applied Physiology, University of Freiburg, FRG.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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