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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1996-12-12
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pubmed:abstractText |
It has been proposed that chronic treatment with growth hormone (GH) or insulin-like growth factor-I (IGF-I) in the rat may enhance cardiac function in vivo. To confirm these findings and elucidate the mechanisms by which cardiac function is modulated, we studied isolated buffer-perfused rat hearts after 4 weeks of treatment with high doses of GH and IGF-I alone or in combination. Mechanical parameters were measured at 50% of the intracardiac balloon volume at which maximal developed pressure (DevP) occurred. EC50 of the force-Ca2+ relationship and maximal Ca(2+)-activated systolic wall stress (max sigma s) were assessed by increasing Ca2+ in the perfusate in a stepwise fashion and plotting systolic wall stress (sigma s) versus intracellular peak systolic Ca2+, measured by the aequorin bioluminescence method. We found a marked increase of systolic pressure (Ps), DevP, and (+dP/dt)/DevP in the treated groups compared with the control group. The combination group showed a blunted effect. sigma s was increased in all treated groups for a perfusate Ca2+ concentration of > 1.5 mmol/L. The enhanced systolic performance can be explained by an increase of the overall Ca2+ responsiveness due to an increased maximal response to Ca2+ even though the EC50 of the Ca(2+)-dose response was also slightly increased. Ps was further enhanced by an increase of the relative wall thickness induced by the treatment. Diastolic pressure, diastolic Ca2+, and the amplitude and time course of the Ca2+ transient were not influenced by any treatment protocol. All treatments caused increases of body and heart weight. These data support the hypothesis that both IGF-I and GH directly affect cardiac performance by altering cardiac geometry as well as by enhancing max sigma s.
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pubmed:grant | |
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 |
Aug
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pubmed:issn |
0009-7330
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
79
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
227-36
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8755999-Animals,
pubmed-meshheading:8755999-Buffers,
pubmed-meshheading:8755999-Calcium,
pubmed-meshheading:8755999-Dose-Response Relationship, Drug,
pubmed-meshheading:8755999-Female,
pubmed-meshheading:8755999-Growth Hormone,
pubmed-meshheading:8755999-Insulin-Like Growth Factor I,
pubmed-meshheading:8755999-Intracellular Membranes,
pubmed-meshheading:8755999-Myocardium,
pubmed-meshheading:8755999-Perfusion,
pubmed-meshheading:8755999-Rats,
pubmed-meshheading:8755999-Rats, Sprague-Dawley,
pubmed-meshheading:8755999-Ventricular Function, Left
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pubmed:year |
1996
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pubmed:articleTitle |
Exogenously administered growth hormone and insulin-like growth factor-I alter intracellular Ca2+ handling and enhance cardiac performance. In vitro evaluation in the isolated isovolumic buffer-perfused rat heart.
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pubmed:affiliation |
Charles A. Dana Research Institute, Department of Medicine, Beth Israel Hospital, Boston, MA 02215, USA.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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