Source:http://linkedlifedata.com/resource/pubmed/id/15191402
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5-6
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pubmed:dateCreated |
2004-6-11
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pubmed:abstractText |
Chronic heart failure (CHF) impairs endothelium-dependent, nitric oxide (NO)-mediated dilation. This decreased dilation may be partly secondary to the chronic decrease in blood flow, but this hypothesis has not yet been tested. Thus, we assessed whether a localized, chronic increase in blood flow in vivo reverses endothelial dysfunction of small arteries in rats with CHF. Two months after coronary artery ligation or sham surgery, second-order side branches of the superior mesenteric artery were ligated in order to obtain persistently elevated blood flow (HF) in the adjacent first-order side branch compared with normal vessels (NF). One month later, responses to acetylcholine and flow-mediated vasodilatation (FMD) were assessed in vitro in an arteriograph. Chronic heart failure induced a decrease in mesenteric blood flow (374 +/- 25 and 305 +/- 27 micro L/min for sham and CHF, respectively; P < 0.05). Neither CHF nor the chronic increase in flow affected the responses to acetylcholine. Chronic heart failure decreased FMD (maximal response in sham and control 34 +/- 6 and 13 +/- 4%, respectively; P < 0.05). Chronic increases in blood flow did not modify FMD in sham, but restored FMD in CHF rats (28 +/- 4%; P < 0.05 vs CHF NF). The restored response was abolished by an inhibitor of NO synthesis (N(G)-nitro-l-arginine). Chronic heart failure did not affect the abundance of mesenteric endothelial NO synthase (eNOS) mRNA. A chronic increase in flow significantly increased the abundance of eNOS mRNA in sham rats, but only moderately and non-significantly in CHF rats. Thus, endothelial dysfunction of small arteries in CHF appears to be largely the consequence of the chronic decrease in flow.
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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:issn |
0305-1870
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
302-5
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:15191402-Acetylcholine,
pubmed-meshheading:15191402-Animals,
pubmed-meshheading:15191402-Blood Flow Velocity,
pubmed-meshheading:15191402-Chronic Disease,
pubmed-meshheading:15191402-Dose-Response Relationship, Drug,
pubmed-meshheading:15191402-Endothelium, Vascular,
pubmed-meshheading:15191402-Heart Failure,
pubmed-meshheading:15191402-Rats,
pubmed-meshheading:15191402-Splanchnic Circulation,
pubmed-meshheading:15191402-Vascular Diseases,
pubmed-meshheading:15191402-Vasodilation
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pubmed:articleTitle |
Chronic decrease in flow contributes to heart failure-induced endothelial dysfunction in rats.
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pubmed:affiliation |
INSERM U644, IFRMP 23, Rouen, France.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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