Linked Life Data

17267548

Source:http://linkedlifedata.com/resource/pubmed/id/17267548

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-6-12
pubmed:abstractText
This study examined Ca(2+) handling mechanisms involved in cardioprotection induced by chronic intermittent hypoxia (CIH) against ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were exposed to 10% inspired O(2) continuously for 6 h daily from 3, 7, and 14 days. In isolated perfused hearts subjected to I/R, CIH-induced cardioprotection was most significant in the 7-day group with less infarct size and lactate dehydrogenase release, compared with the normoxic group. The I/R-induced alterations in diastolic Ca(2+) level, amplitude, time-to-peak, and the decay time of both electrically and caffeine-induced Ca(2+) transients measured by spectrofluorometry in isolated ventricular myocytes of the 7-day CIH group were less than that of the normoxic group, suggesting an involvement of altered Ca(2+) handling of the sarcoplasmic reticulum (SR) and sarcolemma. We further determined the protein expression and activity of (45)Ca(2+) flux of SR-Ca(2+)-ATPase, ryanodine receptor (RyR) and sarcolemmal Na(+)/Ca(2+) exchange (NCX) in ventricular myocytes from the CIH and normoxic groups before and during I/R. There were no changes in expression levels of the Ca(2+)-handling proteins but significant increases in the RyR and NCX activities were remarkable during I/R in the CIH but not the normoxic group. The augmented RyR and NCX activities were abolished, respectively, by PKA inhibitor (0.5 microM KT5720 or 0.5 microM PKI(14-22)) and PKC inhibitor (5 microM chelerythrine chloride or 0.2 microM calphostin C) but not by Ca(2+)/calmodulin-dependent protein kinase II inhibitor KN-93 (1 microM). Thus, CIH confers cardioprotection against I/R injury in rat cardiomyocytes by altered Ca(2+) handling with augmented RyR and NCX activities via protein kinase activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6143
pubmed:author
pubmed:issnType
Print
pubmed:volume
292
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C2046-56
pubmed:meshHeading
pubmed-meshheading:17267548-Animals, pubmed-meshheading:17267548-Anoxia, pubmed-meshheading:17267548-Body Weight, pubmed-meshheading:17267548-Caffeine, pubmed-meshheading:17267548-Calcium, pubmed-meshheading:17267548-Electrophysiology, pubmed-meshheading:17267548-Gene Expression Regulation, pubmed-meshheading:17267548-Heart, pubmed-meshheading:17267548-Heart Ventricles, pubmed-meshheading:17267548-Male, pubmed-meshheading:17267548-Myocytes, Cardiac, pubmed-meshheading:17267548-Organ Size, pubmed-meshheading:17267548-Oxygen, pubmed-meshheading:17267548-Rats, pubmed-meshheading:17267548-Reperfusion Injury, pubmed-meshheading:17267548-Ryanodine Receptor Calcium Release Channel, pubmed-meshheading:17267548-Sarcolemma, pubmed-meshheading:17267548-Sarcoplasmic Reticulum, pubmed-meshheading:17267548-Sarcoplasmic Reticulum Calcium-Transporting ATPases, pubmed-meshheading:17267548-Sodium, pubmed-meshheading:17267548-Sodium-Calcium Exchanger, pubmed-meshheading:17267548-Time Factors
pubmed:year
2007
pubmed:articleTitle
Chronic intermittent hypoxia alters Ca2+ handling in rat cardiomyocytes by augmented Na+/Ca2+ exchange and ryanodine receptor activities in ischemia-reperfusion.
pubmed:affiliation
Dept. of Physiology, University of Hong Kong, Pokfulam, Hong Kong.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't