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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1994-11-10
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pubmed:abstractText |
Previous reports have indicated that the senescent myocardium is less tolerant to surgically induced ischemia and that diminished functional recovery is associated with alterations in cytosolic calcium ([Ca2+]i) accumulation. Recently, increased [Ca2+]i has been suggested to alter nuclear calcium ([Ca2+]n) accumulation. To investigate the relation between [Ca2+]i and [Ca2+]n, we subjected mature and aged rabbit hearts to normothermic global ischemia, either without treatment or after treatment with potassium cardioplegia, magnesium cardioplegia, or a combination of potassium and magnesium cardioplegia. The relation between altered [Ca2+]n and DNA fragmentation was also investigated. Our results indicate that [Ca2+]i was increased during 30 minutes of normothermic global ischemia without treatment in both the mature and aged hearts (p < 0.05). Accumulation of [Ca2+]i during global ischemia was reduced with the use of potassium, magnesium, and a combination of potassium and magnesium cardioplegia (p < 0.05 versus untreated ischemia) in both the mature and aged hearts. Levels of [Ca2+]n were unaffected by global ischemia or cardioplegia in the mature myocardium; however, in the aged myocardium, [Ca2+]n was increased during global ischemia and with potassium cardioplegia and was associated with increased nuclear DNA fragmentation (p < 0.05). The use of magnesium and a combination of potassium and magnesium cardioplegia attenuated [Ca2+]n accumulation and nuclear DNA fragmentation (p < 0.05). Control of [Ca2+]i and [Ca2+]n was associated with enhanced functional recovery during reperfusion. These results indicate that during normothermic ischemia, there is increased [Ca2+]i and [Ca2+]n in the aged myocardium, and increased [Ca2+]n is associated with increased nuclear DNA fragmentation.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0003-4975
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
58
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1005-11
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7944743-Aging,
pubmed-meshheading:7944743-Animals,
pubmed-meshheading:7944743-Calcium,
pubmed-meshheading:7944743-Cell Nucleus,
pubmed-meshheading:7944743-Cytosol,
pubmed-meshheading:7944743-DNA Damage,
pubmed-meshheading:7944743-Heart,
pubmed-meshheading:7944743-Heart Arrest, Induced,
pubmed-meshheading:7944743-Magnesium Sulfate,
pubmed-meshheading:7944743-Myocardium,
pubmed-meshheading:7944743-Potassium Chloride,
pubmed-meshheading:7944743-Rabbits,
pubmed-meshheading:7944743-Ventricular Function, Left
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pubmed:year |
1994
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pubmed:articleTitle |
Magnesium cardioplegia reduces cytosolic and nuclear calcium and DNA fragmentation in the senescent myocardium.
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pubmed:affiliation |
Division of Cardiothoracic Surgery, New England Deaconess Hospital, Boston, Ma 02215.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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