Linked Life Data

17208997

Source:http://linkedlifedata.com/resource/pubmed/id/17208997

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-4-10
pubmed:abstractText
We have previously reported that the prolonged transient acidosis during early reperfusion mediates the cardioprotective effects in canine hearts. Recently, postconditioning has been shown to be one of the novel strategies to mediate cardioprotection. We tested the contribution of the prolonged transient acidosis to the cardioprotection of postconditioning. Open-chest anesthetized dogs subjected to 90-min occlusion of the left anterior descending coronary artery and 6-h reperfusion were divided into four groups: 1) control group; no intervention after reperfusion (n = 6); 2) postconditioning (Postcon) group; four cycles of 1-min reperfusion and 1-min reocclusion (n = 7); 3) Postcon + sodium bicarbonate (NaHCO(3)) group; four cycles of 1-min reperfusion and 1-min reocclusion with the administration of NaHCO(3) (n = 8); and 4) NaHCO(3) group; administration of NaHCO(3) without postconditioning (n = 6). Infarct size, the area at risk (AAR), collateral blood flow during ischemia, and pH in coronary venous blood were measured. The phosphorylation of Akt and extracellular signal-regulated kinase (ERK) in ischemic myocardium was assessed by Western blot analysis. Systemic hemodynamic parameters, AAR, and collateral blood flow were not different among the four groups. Postconditioning induced prolonged transient acidosis during the early reperfusion phase. Administration of NaHCO(3) completely abolished the infarct size-limiting effects of postconditioning. Furthermore, the phosphorylation of Akt and ERK in ischemic myocardium induced by postconditioning was also blunted by the cotreatment of NaHCO(3). In conclusion, postconditioning mediates its cardioprotective effects possibly via prolonged transient acidosis during the early reperfusion phase with the activation of Akt and ERK.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
292
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2004-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17208997-Acidosis, pubmed-meshheading:17208997-Animals, pubmed-meshheading:17208997-Collateral Circulation, pubmed-meshheading:17208997-Coronary Circulation, pubmed-meshheading:17208997-Dogs, pubmed-meshheading:17208997-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:17208997-Hydrogen-Ion Concentration, pubmed-meshheading:17208997-Ischemic Preconditioning, Myocardial, pubmed-meshheading:17208997-MAP Kinase Signaling System, pubmed-meshheading:17208997-Myocardial Infarction, pubmed-meshheading:17208997-Myocardial Reperfusion, pubmed-meshheading:17208997-Myocardial Reperfusion Injury, pubmed-meshheading:17208997-Phosphatidylinositol 3-Kinases, pubmed-meshheading:17208997-Phosphorylation, pubmed-meshheading:17208997-Proto-Oncogene Proteins c-akt, pubmed-meshheading:17208997-Sodium Bicarbonate, pubmed-meshheading:17208997-Veins
pubmed:year
2007
pubmed:articleTitle
Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of postconditioning.
pubmed:affiliation
Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't