| pubmed-article:9746495 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9746495 | lifeskim:mentions | umls-concept:C0018801 | lld:lifeskim |
| pubmed-article:9746495 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:9746495 | lifeskim:mentions | umls-concept:C0596981 | lld:lifeskim |
| pubmed-article:9746495 | lifeskim:mentions | umls-concept:C0019868 | lld:lifeskim |
| pubmed-article:9746495 | lifeskim:mentions | umls-concept:C0205161 | lld:lifeskim |
| pubmed-article:9746495 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:9746495 | pubmed:issue | 4 Pt 2 | lld:pubmed |
| pubmed-article:9746495 | pubmed:dateCreated | 1998-11-19 | lld:pubmed |
| pubmed-article:9746495 | pubmed:abstractText | To determine whether there are abnormalities in myocyte excitation-contraction coupling and intracellular Ca2+ concentration ([Ca2+]i) homeostasis in pacing-induced heart failure (PF), we measured L-type Ca2+ current (ICa,L) and Na+/Ca2+ exchanger current (INa/Ca) with voltage clamp and measured intracellular Na+ concentration ([Na+]i) and [Ca2+]i with the use of sodium-binding benzofuran isophthalate (SBFI) and fluo 3 in ventricular myocytes isolated from control and paced rabbits. The peak systolic and diastolic levels and the amplitude of electrically stimulated [Ca2+]i transients (0.25 Hz, extracellular Ca2+ concentration = 1.08 mM) were significantly less in PF myocytes. Also, there was prolongation of the times to peak and decline of [Ca2+]i transients. ICa,L density was markedly decreased in PF myocytes. INa/Ca at -40 mV elicited by rapid exposure to 0 Na+ solution with a rapid solution switcher was significantly reduced in PF myocytes, suggesting that the function of the Na+/Ca2+ exchanger is impaired in these myocytes. In PF myocytes the decline of the [Ca2+]i transient when the Na+/Ca2+ exchanger was abruptly disabled was markedly prolonged compared with the decline in control myocytes, consistent with depressed sarcoplasmic reticulum (SR) Ca2+-ATPase function. RNase protection assay showed decreased levels of Na+/Ca2+ exchanger and SR Ca2+-ATPase mRNA in PF hearts, consistent with the function studies. We conclude that the functions of L-type Ca2+ channels, Na+/Ca2+ exchanger, and SR Ca2+-ATPase are impaired in myocytes from rabbit hearts with failure induced by rapid pacing. These abnormalities result in reduced [Ca2+]i transients and systolic and diastolic dysfunction and appear to account for the abnormal ventricular function observed. | lld:pubmed |
| pubmed-article:9746495 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9746495 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9746495 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9746495 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9746495 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9746495 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9746495 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9746495 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9746495 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:9746495 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:RossJJJr | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:BarryW HWH | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:SpitzerK WKW | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:PéAA | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:NonakoSS | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:YamCC | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:BridgeJ HJH | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:ZubairII | lld:pubmed |
| pubmed-article:9746495 | pubmed:author | pubmed-author:MuelheimsGG | lld:pubmed |
| pubmed-article:9746495 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9746495 | pubmed:volume | 275 | lld:pubmed |
| pubmed-article:9746495 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9746495 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9746495 | pubmed:pagination | H1441-8 | lld:pubmed |
| pubmed-article:9746495 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:9746495 | pubmed:meshHeading | pubmed-meshheading:9746495-... | lld:pubmed |
| pubmed-article:9746495 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9746495 | pubmed:articleTitle | Abnormal myocyte Ca2+ homeostasis in rabbits with pacing-induced heart failure. | lld:pubmed |
| pubmed-article:9746495 | pubmed:affiliation | Division of Cardiology, University of Utah Health Sciences Center, Salt Lake City, Utah 84132, USA. | lld:pubmed |
| pubmed-article:9746495 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9746495 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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