Source:http://linkedlifedata.com/resource/pubmed/id/15167269
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2004-5-28
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pubmed:abstractText |
Circulating levels of the potent vasoconstrictor peptide endothelin-1 (ET-1) are increased in congestive heart failure (CHF). Coronary blood flow and myocardial oxygen consumption (MVO2) are decreased in some models of CHF. This study tested the hypothesis that ET-1 induced coronary vasoconstriction limits oxygen availability in the failing heart. The effects of selective ET-A receptor blockade with BQ610 (5 microg/min, intracoronary) and selective ET-B receptor blockade with BQ788 (5 microg/min, intracoronary) on coronary blood flow were examined at rest and during graded treadmill exercise in 8 dogs in which congestive heart failure (CHF) had been produced by rapid ventricular pacing for three to four weeks. In animals with CHF, ET-B receptor blockade caused no change in left ventricular (LV) pressure or coronary blood flow. In contrast, ET-A blockade with BQ610 resulted in modest significant increases of coronary blood flow at rest (from 22.4 +/- 2.1 to 27.9 +/- 3.0 mL/min) and during two exercise stages (from 26.9 +/- 2.0 to 30.7 +/- 1.9 during stage 1 exercise and from 28.5 +/- 2.0 to 31.7 +/- 1.3 mL/min during stage 2; all P < 0.05), with an upward shift in the relationship between coronary flow and rate-pressure product. The increase in coronary flow produced by ET-A blockade was not associated with an increase of either myocardial oxygen uptake or LV dP/dt. Thus, although ET-A receptor blockade caused a modest increase in coronary flow, this did not result in an increase of MVO2, implying that ET-A-mediated coronary vasoconstriction did not limit oxygen uptake by the failing heart.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/HL20598,
http://linkedlifedata.com/resource/pubmed/grant/HL21872,
http://linkedlifedata.com/resource/pubmed/grant/R01 HL071790-01A1,
http://linkedlifedata.com/resource/pubmed/grant/R01 HL071790-02,
http://linkedlifedata.com/resource/pubmed/grant/R01 HL071790-03,
http://linkedlifedata.com/resource/pubmed/grant/R01 HL071790-04
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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 |
Jun
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pubmed:issn |
0160-2446
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
764-9
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pubmed:dateRevised |
2011-4-20
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pubmed:meshHeading |
pubmed-meshheading:15167269-Animals,
pubmed-meshheading:15167269-Coronary Circulation,
pubmed-meshheading:15167269-Dogs,
pubmed-meshheading:15167269-Dose-Response Relationship, Drug,
pubmed-meshheading:15167269-Endothelin-1,
pubmed-meshheading:15167269-Heart Failure,
pubmed-meshheading:15167269-Oligopeptides,
pubmed-meshheading:15167269-Receptor, Endothelin A
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pubmed:year |
2004
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pubmed:articleTitle |
ET-A receptor activity restrains coronary blood flow in the failing heart.
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pubmed:affiliation |
Department of Medicine, University of Minnesota Health Sciences Center, Minneapolis, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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