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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1994-6-8
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pubmed:abstractText |
We examined whether prostaglandin (PG) H2, as an endothelium-dependent contracting factor, or the disturbed production of endothelium-derived relaxing factor, impairs endothelium-dependent relaxation and whether long-term inhibition of nitric oxide (NO) synthesis aggravates atherosclerosis in hypercholesterolemic rabbits. Male New Zealand White rabbits were fed one of the following diets: (1) standard chow; (2) 2% cholesterol-supplemented chow; (3) standard chow with 80 micrograms/mL N omega-nitro-L-arginine methylester (L-NAME), an NO synthetase inhibitor, in their drinking water; or (4) 2% cholesterol-supplemented chow with 80 or 160 micrograms/mL L-NAME in their drinking water. The rabbits were fed these diets for 8 or 12 weeks. Then aortic rings were obtained, and changes in isometric tension were recorded. Intimal atherosclerotic areas of the thoracic aortas were subsequently measured by planimetry. The cholesterol-supplemented diet significantly impaired endothelium-dependent aortic relaxation to acetylcholine. Pretreatment with the thromboxane A2/PGH2 receptor antagonist ONO-3708 did not reverse this impaired response. Vessels from both normocholesterolemic and hypercholesterolemic rabbits given L-NAME showed more impaired endothelium-dependent relaxation than those from their dietary counterparts not given L-NAME. Morphometric analysis revealed marked enlargement of intimal atherosclerotic areas in aortas from L-NAME-treated hypercholesterolemic rabbits compared with those from untreated hypercholesterolemic rabbits. These findings suggest that PGH2 does not contribute to impaired endothelium-dependent relaxation and that long-term administration of L-NAME promotes atherosclerosis by inhibition of NO synthesis in the hypercholesterolemic rabbit thoracic aorta.
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pubmed:commentsCorrections | |
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/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin H2,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins H
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1049-8834
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
746-52
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:8172852-Animals,
pubmed-meshheading:8172852-Aorta, Thoracic,
pubmed-meshheading:8172852-Arginine,
pubmed-meshheading:8172852-Arteriosclerosis,
pubmed-meshheading:8172852-Endothelium, Vascular,
pubmed-meshheading:8172852-Hypercholesterolemia,
pubmed-meshheading:8172852-Male,
pubmed-meshheading:8172852-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:8172852-Nitric Oxide,
pubmed-meshheading:8172852-Prostaglandin H2,
pubmed-meshheading:8172852-Prostaglandins H,
pubmed-meshheading:8172852-Rabbits,
pubmed-meshheading:8172852-Vasodilation
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pubmed:year |
1994
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pubmed:articleTitle |
Long-term inhibition of NO synthesis promotes atherosclerosis in the hypercholesterolemic rabbit thoracic aorta. PGH2 does not contribute to impaired endothelium-dependent relaxation.
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pubmed:affiliation |
Department of Internal Medicine II, Nagoya University School of Medicine, Japan.
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pubmed:publicationType |
Journal Article
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