| pubmed-article:7896587 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7896587 | lifeskim:mentions | umls-concept:C1882687 | lld:lifeskim |
| pubmed-article:7896587 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:7896587 | lifeskim:mentions | umls-concept:C0005486 | lld:lifeskim |
| pubmed-article:7896587 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:7896587 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:7896587 | pubmed:dateCreated | 1995-4-21 | lld:pubmed |
| pubmed-article:7896587 | pubmed:abstractText | Assessing the role of O2 supply in the regulation of cardiac function in O2-limited hearts is crucial to understanding myocardial ischemic preconditioning and adaptation to hypoxia. We exposed isolated Langendorff-perfused rat hearts to either ischemia (low coronary flow) or hypoxemia (low PO2 in the perfusing medium) with matched O2 supply (10% of baseline). Myocardial contractile work and ATP turnover were greater in hypoxemic than in ischemic hearts (P < 0.05; n = 12). Thus, the energy demand was higher during hypoxemia than during ischemia, suggesting that ischemic hearts are more downregulated than hypoxemic hearts. Venous PO2 was 12 +/- 2 and 120 +/- 15 Torr (P < 0.0001) for ischemic and hypoxemic hearts, respectively, but O2 uptake was the same. Lactate release was higher during hypoxemia than during ischemia (9.7 +/- 0.9 vs. 1.4 +/- 0.2 mumol/min, respectively; P < 0.0001). Electrical stimulation (300 min-1; to increase energy demand) increased performance in ischemic (P < 0.005) but not in hypoxemic hearts without changes in venous PO2 or O2 uptake. However, venous lactate concentration and lactate release increased in ischemic (P < 0.002) but not in hypoxemic hearts, suggesting that anaerobic glycolysis provides the energy necessary to meet the increased energy demand in ischemic hearts only. We conclude that high intracellular lactate or H+ concentration during ischemia plays a major role as a downregulating factor. Downregulation disappears in hypoxemic hearts secondary to enhanced washout of lactate or H+. | lld:pubmed |
| pubmed-article:7896587 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7896587 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7896587 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7896587 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7896587 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7896587 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:7896587 | pubmed:issn | 8750-7587 | lld:pubmed |
| pubmed-article:7896587 | pubmed:author | pubmed-author:SamajaMM | lld:pubmed |
| pubmed-article:7896587 | pubmed:author | pubmed-author:ChierchiaS... | lld:pubmed |
| pubmed-article:7896587 | pubmed:author | pubmed-author:AllibardiSS | lld:pubmed |
| pubmed-article:7896587 | pubmed:author | pubmed-author:CasaliniSS | lld:pubmed |
| pubmed-article:7896587 | pubmed:author | pubmed-author:CornsMM | lld:pubmed |
| pubmed-article:7896587 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7896587 | pubmed:volume | 77 | lld:pubmed |
| pubmed-article:7896587 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7896587 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7896587 | pubmed:pagination | 2530-6 | lld:pubmed |
| pubmed-article:7896587 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:meshHeading | pubmed-meshheading:7896587-... | lld:pubmed |
| pubmed-article:7896587 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7896587 | pubmed:articleTitle | Regulation of bioenergetics in O2-limited isolated rat hearts. | lld:pubmed |
| pubmed-article:7896587 | pubmed:affiliation | Department of Biomedical Science and Technology, Scientific Institute San Raffaele, University of Milan, San Donato Hospital, Italy. | lld:pubmed |
| pubmed-article:7896587 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7896587 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:7896587 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:7896587 | lld:pubmed |
