Linked Life Data

15556168

Source:http://linkedlifedata.com/resource/pubmed/id/15556168

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-11-23
pubmed:abstractText
Adaptation to intermittent high altitude (IHA) hypoxia can protect the heart against ischemia-reperfusion injury. In view of the fact that both Ca2+ paradox and ischemia-reperfusion injury are associated with the intracellular Ca2+ overload, we tested the hypothesis that IHA hypoxia may protect hearts against Ca2+ paradox-induced lethal injury if its cardioprotection bases on preventing the development of intracellular Ca2+ overload. Langendorff-perfused hearts from normoxic and IHA hypoxic rats were subjected to Ca2+ paradox (5 min of Ca2+ depletion followed by 30 min of Ca2+ repletion) and the functional, biochemical and pathological changes were investigated. The Ca2+ paradox incapacitated the contractility of the normoxic hearts, whereas the IHA hypoxic hearts significantly preserved contractile activity. Furthermore, the normoxic hearts subjected to Ca2+ paradox exhibited a marked reduction in coronary flow, increase in lactate dehydrogenase release, and severe myocyte damage. In contrast, these changes were significantly prevented in IHA hypoxic hearts. We, then, tested and confirmed our hypothesis that the protective mechanisms are mediated by mitochondria ATP-sensitive potassium channels (mitoKATP) and Ca2+/calmodulin-dependent protein kinase II (CaMKII), as the protective effect of IHA hypoxia was abolished by 5-hydroxydecanoate, a selective mitoKATP blocker, and significantly attenuated by KN-93, a CaMKII inhibitor. In conclusion, our studies offer for the first time that IHA hypoxia confers cardioprotection against the lethal injury of Ca2+ paradox and give biochemical evidence for the protective mechanism of IHA hypoxia. We propose that researches in this area may lead a preventive regimen against myocardial injury associated with Ca2+ overload.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
559-72
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:15556168-Adaptation, Physiological, pubmed-meshheading:15556168-Altitude, pubmed-meshheading:15556168-Animals, pubmed-meshheading:15556168-Anoxia, pubmed-meshheading:15556168-Body Weight, pubmed-meshheading:15556168-Calcium, pubmed-meshheading:15556168-Calcium-Calmodulin-Dependent Protein Kinase Type 2, pubmed-meshheading:15556168-Calcium-Calmodulin-Dependent Protein Kinases, pubmed-meshheading:15556168-L-Lactate Dehydrogenase, pubmed-meshheading:15556168-Male, pubmed-meshheading:15556168-Myocardial Reperfusion Injury, pubmed-meshheading:15556168-Myocardium, pubmed-meshheading:15556168-Organ Size, pubmed-meshheading:15556168-Potassium Channels, pubmed-meshheading:15556168-Rats, pubmed-meshheading:15556168-Rats, Sprague-Dawley, pubmed-meshheading:15556168-Time Factors, pubmed-meshheading:15556168-Ventricular Function, Left
pubmed:year
2004
pubmed:articleTitle
Intermittent high altitude hypoxia protects the heart against lethal Ca2+ overload injury.
pubmed:affiliation
Laboratory of Molecular Cardiology, Health Science Center, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, 225 Chong Qing Nan Rd, Build. #1, Shanghai, 200025, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't