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pubmed-article:7834837pubmed:abstractTextA 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.lld:pubmed
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pubmed-article:7834837pubmed:authorpubmed-author:WoodcockE AEAlld:pubmed
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pubmed-article:7834837pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:7834837pubmed:articleTitleInositol phosphate release and metabolism during myocardial ischemia and reperfusion in rat heart.lld:pubmed
pubmed-article:7834837pubmed:affiliationCellular Biochemistry Laboratory, Baker Medical Research Institute, Prahran, Australia.lld:pubmed
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pubmed-article:7834837pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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