pubmed-article:15044191 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15044191 | lifeskim:mentions | umls-concept:C0022116 | lld:lifeskim |
pubmed-article:15044191 | lifeskim:mentions | umls-concept:C1955862 | lld:lifeskim |
pubmed-article:15044191 | lifeskim:mentions | umls-concept:C0005802 | lld:lifeskim |
pubmed-article:15044191 | lifeskim:mentions | umls-concept:C0439857 | lld:lifeskim |
pubmed-article:15044191 | lifeskim:mentions | umls-concept:C0427743 | lld:lifeskim |
pubmed-article:15044191 | lifeskim:mentions | umls-concept:C1287281 | lld:lifeskim |
pubmed-article:15044191 | lifeskim:mentions | umls-concept:C1882151 | lld:lifeskim |
pubmed-article:15044191 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:15044191 | pubmed:dateCreated | 2004-7-27 | lld:pubmed |
pubmed-article:15044191 | pubmed:abstractText | We tested the hypothesis that glucose-insulin-potassium (GIK)-induced protection against myocardial infarction depends on ATP-dependent K(+) (K(ATP)) channel activation and is abolished by hyperglycemia before the ischemia. Dogs were subjected to a 60-min coronary artery occlusion and 3-h reperfusion in the absence or presence of GIK (25% dextrose; 50 IU insulin/l; 80 mM/l KCl infused at 1.5 ml x kg(-1) x h(-1)) beginning 75 min before coronary artery occlusion or 5 min before reperfusion. The role of K(ATP) channels was evaluated by pretreatment with glyburide (0.1 mg/kg). The efficacy of GIK was investigated with increases in blood glucose (BG) concentrations to 300 or 600 mg/dl or experimental diabetes (alloxan/streptozotocin). Infarct size (IS) was 29 +/- 2% of the area at risk in control experiments. GIK decreased (P < 0.05) IS when administered beginning 5 min before reperfusion. This protective action was independent of BG (13 +/- 2 and 12 +/- 2% of area at risk; BG = 80 or 600 mg/dl, respectively) but was abolished in dogs receiving glyburide (30 +/- 4%), hyperglycemia before ischemia (27 +/- 4%), or diabetes (25 +/- 3%). IS was unchanged by GIK when administered before ischemia independent of BG (31 +/- 3, 27 +/- 2, and 35 +/- 3%; BG = 80, 300, and 600 mg/dl, respectively). The insulin component of GIK promotes cardioprotection by K(ATP) channel activation. However, glucose decreases K(ATP) channel activity, and this effect predominates when hyperglycemia is present before ischemia. | lld:pubmed |
pubmed-article:15044191 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:language | eng | lld:pubmed |
pubmed-article:15044191 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15044191 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15044191 | pubmed:month | Aug | lld:pubmed |
pubmed-article:15044191 | pubmed:issn | 0363-6135 | lld:pubmed |
pubmed-article:15044191 | pubmed:author | pubmed-author:KrolikowskiJo... | lld:pubmed |
pubmed-article:15044191 | pubmed:author | pubmed-author:PagelPaul SPS | lld:pubmed |
pubmed-article:15044191 | pubmed:author | pubmed-author:WarltierDavid... | lld:pubmed |
pubmed-article:15044191 | pubmed:author | pubmed-author:KerstenJudy... | lld:pubmed |
pubmed-article:15044191 | pubmed:author | pubmed-author:LaDisaJohn... | lld:pubmed |
pubmed-article:15044191 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15044191 | pubmed:volume | 287 | lld:pubmed |
pubmed-article:15044191 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15044191 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15044191 | pubmed:pagination | H601-7 | lld:pubmed |
pubmed-article:15044191 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:15044191 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15044191 | pubmed:articleTitle | Cardioprotection by glucose-insulin-potassium: dependence on KATP channel opening and blood glucose concentration before ischemia. | lld:pubmed |
pubmed-article:15044191 | pubmed:affiliation | Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. | lld:pubmed |
pubmed-article:15044191 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15044191 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15044191 | lld:pubmed |