Linked Life Data

16306124

Source:http://linkedlifedata.com/resource/pubmed/id/16306124

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-3-13
pubmed:abstractText
We have previously demonstrated that intermittent high-altitude (IHA) hypoxia significantly attenuates ischemia-reperfusion (I/R) injury-induced excessive increase in resting intracellular Ca(2+) concentrations ([Ca(2+)](i)). Because the sarcoplasmic reticulum (SR) and Na(+)/Ca(2+) exchanger (NCX) play crucial roles in regulating [Ca(2+)](i) and both are dysfunctional during I/R, we tested the hypothesis that IHA hypoxia may prevent I/R-induced Ca(2+) overload by maintaining Ca(2+) homeostasis via SR and NCX mechanisms. We thus determined the dynamics of Ca(2+) transients and cell shortening during preischemia and I/R injury in ventricular cardiomyocytes from normoxic and IHA hypoxic rats. IHA hypoxia did not affect the preischemic dynamics of Ca(2+) transients and cell shortening, but it significantly suppressed the I/R-induced increase in resting [Ca(2+)](i) levels and attenuated the depression of the Ca(2+) transients and cell shortening during reperfusion. Moreover, IHA hypoxia significantly attenuated I/R-induced depression of the protein contents of SR Ca(2+) release channels and/or ryanodine receptors (RyRs) and SR Ca(2+) pump ATPase (SERCA2) and SR Ca(2+) release and uptake. In addition, a delayed decay rate time constant of Ca(2+) transients and cell shortening of Ca(2+) transients observed during ischemia was accompanied by markedly inhibited NCX currents, which were prevented by IHA hypoxia. These findings indicate that IHA hypoxia may preserve Ca(2+) homeostasis and contraction by preserving RyRs and SERCA2 proteins as well as NCX activity during I/R.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0363-6143
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C1221-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16306124-Altitude, pubmed-meshheading:16306124-Animals, pubmed-meshheading:16306124-Anoxia, pubmed-meshheading:16306124-Caffeine, pubmed-meshheading:16306124-Calcium, pubmed-meshheading:16306124-Calcium-Transporting ATPases, pubmed-meshheading:16306124-Homeostasis, pubmed-meshheading:16306124-Male, pubmed-meshheading:16306124-Muscle Contraction, pubmed-meshheading:16306124-Myocytes, Cardiac, pubmed-meshheading:16306124-Patch-Clamp Techniques, pubmed-meshheading:16306124-Rats, pubmed-meshheading:16306124-Rats, Sprague-Dawley, pubmed-meshheading:16306124-Reperfusion Injury, pubmed-meshheading:16306124-Ryanodine Receptor Calcium Release Channel, pubmed-meshheading:16306124-Sarcoplasmic Reticulum, pubmed-meshheading:16306124-Sarcoplasmic Reticulum Calcium-Transporting ATPases, pubmed-meshheading:16306124-Sodium, pubmed-meshheading:16306124-Sodium-Calcium Exchanger
pubmed:year
2006
pubmed:articleTitle
Intermittent hypoxia protects cardiomyocytes against ischemia-reperfusion injury-induced alterations in Ca2+ homeostasis and contraction via the sarcoplasmic reticulum and Na+/Ca2+ exchange mechanisms.
pubmed:affiliation
Laboratory of Molecular Cardiology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine, 225 Chong Qing Nan Rd., #1 Bldg., Shanghai 200025, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't