Source:http://linkedlifedata.com/resource/pubmed/id/14508241
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2003-9-25
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pubmed:abstractText |
The authors examined effects of positive (dopamine and digoxin) and negative (nifedipine and lidocaine) inotropic interventions on the instantaneous cyclic relationship between myoplasmic [Ca2+] and simultaneously developed left ventricular pressure (LVP) in intact guinea pig hearts. Novel indices were developed to quantify this relationship based on (1) transient [Ca2+] and LVP signal morphology, ie, maxima and minima, peak derivatives, beat areas, durations, and ratios of indices of LVP to [Ca2+]; (2) temporal delay; and (3) LVP versus [Ca2+] loop morphology, ie, orientation, size, hysteresis, position, shape, and duration. These analyses were used to assess the cost of phasic [Ca2+] for contraction and relaxation over one beat after inotropic intervention. It was found that dopamine and digoxin increased contractile and relaxation responsiveness to phasic [Ca2+], cumulative Ca2+, and net Ca2+ flux. Unlike dopamine, digoxin did not decrease relaxation response time. Nifedipine and lidocaine decreased contractile and relaxation responsiveness to phasic [Ca2+], cumulative Ca2+, and net Ca2+ flux. Unlike lidocaine, nifedipine decreased net available Ca2+ and Ca2+ influx. Positive inotropic agents increased [Ca2+]-LVP loop area and hysteresis and resulted in a more vertically oriented loop. Nifedipine and lidocaine decreased these loop indices and lidocaine exhibited greater loop hysteresis than did nifedipine. These novel indices provide a quantitative assessment of myoplasmic [Ca2+] handling for cardiac contractile function.
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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 |
Oct
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pubmed:issn |
0160-2446
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
42
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
539-53
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:14508241-Animals,
pubmed-meshheading:14508241-Calcium,
pubmed-meshheading:14508241-Digoxin,
pubmed-meshheading:14508241-Dopamine,
pubmed-meshheading:14508241-Guinea Pigs,
pubmed-meshheading:14508241-Lidocaine,
pubmed-meshheading:14508241-Muscle Contraction,
pubmed-meshheading:14508241-Myocardial Contraction,
pubmed-meshheading:14508241-Myocardium,
pubmed-meshheading:14508241-Nifedipine,
pubmed-meshheading:14508241-Signal Processing, Computer-Assisted,
pubmed-meshheading:14508241-Ventricular Function,
pubmed-meshheading:14508241-Ventricular Function, Left,
pubmed-meshheading:14508241-Ventricular Pressure
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pubmed:year |
2003
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pubmed:articleTitle |
How inotropic drugs alter dynamic and static indices of cyclic myoplasmic [Ca2+] to contractility relationships in intact hearts.
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pubmed:affiliation |
Department of Biomedical Engineering, Marquette University, Milwaukee, Wisconsin, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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