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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5 Pt 2
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pubmed:dateCreated |
1995-7-6
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pubmed:abstractText |
Gadolinium-sensitive stretch-activated channels have been implicated in the process of mechanotransduction signaling of ventricular myocardium. Such channels nonspecifically transport Na+ and Ca2+ in the inward direction. We tested the hypothesis that Na+ and Ca2+ influx are important in the genesis of stretch-induced arrhythmias (SIAs) in an isolated, blood-perfused canine ventricle. To elicit SIAs, left ventricular volume was transiently increased in early diastole using a computerized servo-pump system. Monophasic action potential recordings revealed stretch-induced depolarizations (SIDs) that preceded the arrhythmias. In five ventricles, raising the perfusate Ca2+ concentration from 1 to 3 mM increased ventricular sensitivity to SIAs, manifested by a decrease in the volume change required to precipitate an arrhythmia 50% of the time (delta V50) from 19.5 +/- 2.7 to 15.2 +/- 1.9 ml (P < 0.05). When the perfusate Na+ concentration was decreased from 150 to 90 mM in seven ventricles, delta V50 greatly increased (31.1 +/- 14.4 vs. 17.7 +/- 5.3 ml, P < 0.05), and SID amplitude decreased by 47% (P = 0.002). The suppression of SIAs with low extracellular Na+ is unlikely to be mediated by voltage-gated Na+ channels because lidocaine (5 mg/dl) did not alter SID amplitude. Thus the transsarcolemmal Na+ gradient (and probably that of Ca2+) modulates the amplitude of SIDs, which, in turn, initiate SIAs. These data provide initial evidence that Na+ and Ca2+ help mediate the mechanotransduction processes that underly the genesis of SIAs.
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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 |
May
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
268
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H1803-13
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:7771531-Animals,
pubmed-meshheading:7771531-Arrhythmias, Cardiac,
pubmed-meshheading:7771531-Calcium,
pubmed-meshheading:7771531-Dogs,
pubmed-meshheading:7771531-Electrophysiology,
pubmed-meshheading:7771531-Hemodynamics,
pubmed-meshheading:7771531-Lidocaine,
pubmed-meshheading:7771531-Myocardial Contraction,
pubmed-meshheading:7771531-Osmolar Concentration,
pubmed-meshheading:7771531-Rats,
pubmed-meshheading:7771531-Sodium,
pubmed-meshheading:7771531-Ventricular Function
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pubmed:year |
1995
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pubmed:articleTitle |
Calcium- and sodium-dependent modulation of stretch-induced arrhythmias in isolated canine ventricles.
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pubmed:affiliation |
Division of Cardiology, Vanderbilt University Medical School, Nashville, Tennessee 37232, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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