| pubmed-article:1822531 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1822531 | lifeskim:mentions | umls-concept:C0999699 | lld:lifeskim |
| pubmed-article:1822531 | lifeskim:mentions | umls-concept:C2339371 | lld:lifeskim |
| pubmed-article:1822531 | lifeskim:mentions | umls-concept:C0231174 | lld:lifeskim |
| pubmed-article:1822531 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:1822531 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
| pubmed-article:1822531 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:1822531 | pubmed:dateCreated | 1992-9-2 | lld:pubmed |
| pubmed-article:1822531 | pubmed:abstractText | 1. The effects of complete metabolic inhibition on excitation-contraction coupling in heart were studied by exposing patch-clamped guinea-pig ventricular myocytes, loaded via the patch pipette with the Ca2+ indicator Fura-2 (0.1 mM), to carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP, 1 microM) and 2-deoxyglucose (2-DG, 10 mM) while simultaneously recording membrane current, Fura-2 fluorescence, and cell motion. The patch pipette solution contained Cs+ and TEA (tetraethylammonium) to partially block K+ currents. 2. During voltage clamps from a holding potential of -40 mV to a test potential of 0 mV, complete metabolic inhibition decreased the Ca2+ current (ICa), activated the ATP-sensitive K+ current, modestly elevated diastolic [Ca2+]i and markedly reduced the [Ca2+]i transient without altering its voltage dependence. Active shortening was impaired and diastolic cell length decreased prior to large increases in diastolic [Ca2+]i, consistent with rigor induced by ATP depletion. Return of the [Ca2+]i transient to baseline and relaxation upon repolarization were also delayed. 3. Despite the depression of the peak [Ca2+]i transient induced by membrane depolarization during metabolic inhibition, the [Ca2+]i transient induced by a rapid exposure to 5 mM-caffeine was greater than control. The Na(+)-Ca2+ exchange current during the caffeine-induced [Ca2+]i transient was not affected by metabolic inhibition. 4. [Ca2+]i transients depressed by metabolic inhibition could be enhanced by augmenting ICa with elevated [Ca2+]o (10 mM) and Bay K 8644 (5 microM). 5. To study the relationship between the magnitude of ICa and the amplitude of the [Ca2+]i transient, ICa was modulated either by (a) voltage clamping the cell to different membrane potentials at constant [Ca2+]o or by (b) rapidly altering [Ca2+]o immediately prior to a voltage clamp to a fixed membrane potential. Under control conditions, the relationship between the size of ICa and the magnitude of the [Ca2+]i transient was the same whether ICa was modulated by altering membrane potential or [Ca2+]o, suggesting that membrane potential does not significantly modulate the Ca(2+)-induced Ca2+ release mechanism of cardiac excitation-contraction coupling. 6. After metabolic inhibition, however, the same ICa released less Ca2+ than under control conditions, consistent with some impairment of the Ca2+ release mechanism. 7. These results suggest that under conditions in which excitability is maintained by controlling membrane voltage and minimizing metabolically sensitive K+ currents, the decreased [Ca2+]i transient observed during metabolic inhibition severe enough to induce rigor is caused primarily by depression of ICa and not by depletion of intracellular Ca2+ stores. Additional factors also modestly hinder Ca2+ release from intracellular stores during metabolic inhibition. | lld:pubmed |
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| pubmed-article:1822531 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1822531 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1822531 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1822531 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:1822531 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:1822531 | pubmed:author | pubmed-author:ParkerJ MJM | lld:pubmed |
| pubmed-article:1822531 | pubmed:author | pubmed-author:WeissJ NJN | lld:pubmed |
| pubmed-article:1822531 | pubmed:author | pubmed-author:GoldhaberJ... | lld:pubmed |
| pubmed-article:1822531 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1822531 | pubmed:volume | 443 | lld:pubmed |
| pubmed-article:1822531 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1822531 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1822531 | pubmed:pagination | 371-86 | lld:pubmed |
| pubmed-article:1822531 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1822531 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1822531 | pubmed:articleTitle | Mechanisms of excitation-contraction coupling failure during metabolic inhibition in guinea-pig ventricular myocytes. | lld:pubmed |
| pubmed-article:1822531 | pubmed:affiliation | Division of Cardiology, UCLA School of Medicine 90024. | lld:pubmed |
| pubmed-article:1822531 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1822531 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1822531 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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