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rdf:type |
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lifeskim:mentions |
umls-concept:C0015688,
umls-concept:C0028128,
umls-concept:C0035820,
umls-concept:C0042401,
umls-concept:C0085862,
umls-concept:C0086418,
umls-concept:C0205250,
umls-concept:C0214230,
umls-concept:C0332120,
umls-concept:C1299583,
umls-concept:C1549571,
umls-concept:C1608386
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pubmed:issue |
1
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pubmed:dateCreated |
2003-7-15
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pubmed:abstractText |
To evaluate the role of elevation of non-esterified fatty acids on forearm nitric oxide (NO) dependent and independent relaxation, four studies were performed in the forearms of 14 normals: (1). endothelium-dependent and -independent vasodilations were assessed during acetylcholine (Ach) and sodium nitroprusside (SNP) infusions; (2). flow-mediated vasodilation (FMD) was assessed; (3) .bradykinin (BK) was infused during NO and prostaglandin inhibition (NO clamp); (4). blood flow (FBF) was measured during Ouabain, a Na(+)/K(+) ATPase, and BaCl(2), rectifying potassium channel (K(IR)) blockers, respectively. All studies were performed before and after 120 min. Intralipid+heparin (high-NEFA) infusion. Ach-mediated FBF increase was lower at high-NEFA (332+/-34 vs. 436+/-44% at 45 microg l forearm(-1) min(-1); % of ratio infused: control arm P<0.05), while SNP response was similar. FMD did not differ before and during high-NEFA, which induced a blunted response of FBF during BK with or without NO clamp. Ouabain and BaCl(2)-mediated FBF inhibition was lower (P<0.01) at high-NEFA. During ouabain alone FBF decreased slightly. IN CONCLUSION: High-NEFA exerts a negative role on both NO-dependent and independent vasodilations. The decrease in FBF, mediated by K(IR) inhibition, is blunted by high-NEFA: these substrates interfere with hemodynamic/metabolism coupling, possibly through the inhibition of these channels.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Bradykinin,
http://linkedlifedata.com/resource/pubmed/chemical/Fat Emulsions, Intravenous,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside,
http://linkedlifedata.com/resource/pubmed/chemical/Ouabain,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Inwardly...,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin-Endoperoxide Synthases,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0021-9150
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
169
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
147-53
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:12860261-Acetylcholine,
pubmed-meshheading:12860261-Adult,
pubmed-meshheading:12860261-Blood Flow Velocity,
pubmed-meshheading:12860261-Bradykinin,
pubmed-meshheading:12860261-Endothelium, Vascular,
pubmed-meshheading:12860261-Fat Emulsions, Intravenous,
pubmed-meshheading:12860261-Fatty Acids, Nonesterified,
pubmed-meshheading:12860261-Female,
pubmed-meshheading:12860261-Forearm,
pubmed-meshheading:12860261-Humans,
pubmed-meshheading:12860261-Male,
pubmed-meshheading:12860261-Nitric Oxide,
pubmed-meshheading:12860261-Nitric Oxide Synthase,
pubmed-meshheading:12860261-Nitroprusside,
pubmed-meshheading:12860261-Ouabain,
pubmed-meshheading:12860261-Potassium Channels, Inwardly Rectifying,
pubmed-meshheading:12860261-Prostaglandin-Endoperoxide Synthases,
pubmed-meshheading:12860261-Vasodilation,
pubmed-meshheading:12860261-Vasodilator Agents
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pubmed:year |
2003
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pubmed:articleTitle |
Elevated non-esterified fatty acids impair nitric oxide independent vasodilation, in humans: evidence for a role of inwardly rectifying potassium channels.
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pubmed:affiliation |
Department of Clinical and Experimental Medicine, Cattedra di Malattie del Metabolismo, University of Padova, Via Giustiniani 2, 35128 Padua, Italy.
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pubmed:publicationType |
Journal Article
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