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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1995-2-28
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pubmed:abstractText |
A detailed study of the effects of global myocardial ischemia and reperfusion on inositol phosphate release and metabolism has been undertaken by using isolated perfused rat hearts. Ischemia for longer than 5 minutes caused a cessation of inositol phosphate production, with inositol phosphates initially present accumulating as isomers of inositol monophosphate. This inhibition was independent of norepinephrine. In contrast, 2-minute reperfusion following 20-minute ischemia produced a rapid and transient release of inositol phosphates that was dependent on the release of norepinephrine and mediated by alpha 1-adrenergic receptors. By a number of criteria, this reperfusion response was different from the norepinephrine response in normoxic tissue. First, total release of inositol phosphates was greater (466 +/- 37 compared with 345 +/- 29 cpm/mg protein, P < .05). Second, inositol 1,4,5-trisphosphate was released with postischemic reperfusion (103 +/- 18 to 207 +/- 11 pmol/mg protein), whereas release was not detected in normoxic myocardium. In agreement with this, neomycin (0.5 and 5 mmol/L) inhibited inositol phosphate release only under reperfusion conditions. Third, the reperfusion response, unlike the response in nonischemic tissue, required extracellular Ca2+. Longer periods of reperfusion resulted in a return to a pattern of inositol phosphate release that was not different from that seen in normoxic tissue. The rapid and transient release of inositol 1,4,5-trisphosphate at 2-minute postischemic reperfusion provides an explanation for the enhanced role of alpha 1-adrenergic receptors under these conditions and suggests an important role for this compound in initiating reperfusion-induced pathological events.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0009-7330
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
76
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
261-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7834837-Animals,
pubmed-meshheading:7834837-Calcium,
pubmed-meshheading:7834837-Inositol Phosphates,
pubmed-meshheading:7834837-Male,
pubmed-meshheading:7834837-Myocardial Ischemia,
pubmed-meshheading:7834837-Myocardial Reperfusion,
pubmed-meshheading:7834837-Myocardium,
pubmed-meshheading:7834837-Neomycin,
pubmed-meshheading:7834837-Norepinephrine,
pubmed-meshheading:7834837-Rats,
pubmed-meshheading:7834837-Rats, Sprague-Dawley,
pubmed-meshheading:7834837-Time Factors
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pubmed:year |
1995
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pubmed:articleTitle |
Inositol phosphate release and metabolism during myocardial ischemia and reperfusion in rat heart.
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pubmed:affiliation |
Cellular Biochemistry Laboratory, Baker Medical Research Institute, Prahran, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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