Linked Life Data

15242834

Source:http://linkedlifedata.com/resource/pubmed/id/15242834

Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:15242834rdf:typepubmed:Citationlld:pubmed
pubmed-article:15242834lifeskim:mentionsumls-concept:C0006675lld:lifeskim
pubmed-article:15242834lifeskim:mentionsumls-concept:C0035203lld:lifeskim
pubmed-article:15242834lifeskim:mentionsumls-concept:C1510421lld:lifeskim
pubmed-article:15242834lifeskim:mentionsumls-concept:C0449468lld:lifeskim
pubmed-article:15242834lifeskim:mentionsumls-concept:C1709059lld:lifeskim
pubmed-article:15242834lifeskim:mentionsumls-concept:C2349975lld:lifeskim
pubmed-article:15242834lifeskim:mentionsumls-concept:C1882151lld:lifeskim
pubmed-article:15242834lifeskim:mentionsumls-concept:C0764439lld:lifeskim
pubmed-article:15242834pubmed:issue5lld:pubmed
pubmed-article:15242834pubmed:dateCreated2004-10-11lld:pubmed
pubmed-article:15242834pubmed:abstractTextPreviously, we have shown that the pharmacological opening of the mitochondrial ATP-sensitive K channels with diazoxide (DZX) enhances the cardioprotection afforded by magnesium-supplemented potassium (K/Mg) cardioplegia. To determine the mechanisms involved in the cardioprotection afforded by K/Mg + DZX cardioplegia, rabbit hearts (n=24) were subjected to isolated Langendorff perfusion. Control hearts were perfused for 75 min. Global ischemia (GI) hearts were subjected to 30 min of equilibrium, 30 min of GI, and 15 min of reperfusion. K/Mg and K/Mg + DZX cardioplegia hearts received either K/Mg or K/Mg + DZX for 5 min before GI and reperfusion. Tissue was harvested for mitochondrial isolation and transmission electron microscopy (TEM). Mitochondrial structure, area, matrix volume, free calcium, and oxygen consumption were determined. TEM demonstrated that GI mitochondria were damaged and that K/Mg and K/Mg + DZX preserved mitochondrial structure. TEM and light scattering demonstrated separately that mitochondrial matrix and cristae area and matrix volume were significantly increased after GI and reperfusion with GI > K/Mg + DZX > K/Mg hearts (P <0.05 vs. control). Mitochondrial free calcium was significantly increased in GI and K/Mg hearts. K/Mg + DZX significantly decreased mitochondrial free calcium accumulation (P <0.05 vs. GI and K/Mg). State 3 oxygen consumption and respiratory control index in malate (complex I substrate)- and succinate (complex II substrate)-energized mitochondria were significantly decreased (P <0.05 vs. control) in the GI and K/Mg + DZX groups. These data indicate that the enhanced cardioprotection afforded by K/Mg + DZX cardioplegia occurs through the preservation of mitochondrial structure and the significant decrease in mitochondrial free calcium accumulation and mitochondrial state 3 oxygen consumption.lld:pubmed
pubmed-article:15242834pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:languageenglld:pubmed
pubmed-article:15242834pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:citationSubsetIMlld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15242834pubmed:statusMEDLINElld:pubmed
pubmed-article:15242834pubmed:monthNovlld:pubmed
pubmed-article:15242834pubmed:issn0363-6135lld:pubmed
pubmed-article:15242834pubmed:authorpubmed-author:McCullyJames...lld:pubmed
pubmed-article:15242834pubmed:authorpubmed-author:LevitskySidne...lld:pubmed
pubmed-article:15242834pubmed:authorpubmed-author:FedermanMiche...lld:pubmed
pubmed-article:15242834pubmed:authorpubmed-author:RousouAnthony...lld:pubmed
pubmed-article:15242834pubmed:authorpubmed-author:EricssonMaria...lld:pubmed
pubmed-article:15242834pubmed:issnTypePrintlld:pubmed
pubmed-article:15242834pubmed:volume287lld:pubmed
pubmed-article:15242834pubmed:ownerNLMlld:pubmed
pubmed-article:15242834pubmed:authorsCompleteYlld:pubmed
pubmed-article:15242834pubmed:paginationH1967-76lld:pubmed
pubmed-article:15242834pubmed:dateRevised2007-11-14lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:meshHeadingpubmed-meshheading:15242834...lld:pubmed
pubmed-article:15242834pubmed:year2004lld:pubmed
pubmed-article:15242834pubmed:articleTitleOpening of mitochondrial KATP channels enhances cardioprotection through the modulation of mitochondrial matrix volume, calcium accumulation, and respiration.lld:pubmed
pubmed-article:15242834pubmed:affiliationDiv. of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, 77 Ave. Louis Pasteur, Rm. 144, Boston, MA 02115, USA.lld:pubmed
pubmed-article:15242834pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15242834pubmed:publicationTypeIn Vitrolld:pubmed
pubmed-article:15242834pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:15242834lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:15242834lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:15242834lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:15242834lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:15242834lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:15242834lld:pubmed