| The late phase of preconditioning. | |
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MedLine Citation:
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PMID: 11090541 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Unlike the early phase of preconditioning (PC), which lasts 2 to 3 hours and protects against infarction but not against stunning, the late phase of PC lasts 3 to 4 days and protects against both infarction and stunning, suggesting that it may have greater clinical relevance. It is now clear that late PC is a polygenic phenomenon that requires the simultaneous activation of multiple stress-responsive genes. Chemical signals released by a sublethal ischemic stress (such as NO, reactive oxygen species, and adenosine) trigger a complex cascade of signaling events that includes the activation of protein kinase C, Src protein tyrosine kinases, and nuclear factor kappaB and culminates in increased synthesis of inducible NO synthase, cyclooxygenase-2, aldose reductase, Mn superoxide dismutase, and probably other cardioprotective proteins. An analogous sequence of events can be triggered by a variety of stimuli, such as heat stress, exercise, and cytokines. Thus, late PC appears to be a universal response of the heart to stress in general. Importantly, the cardioprotective effects of late PC can be reproduced pharmacologically with clinically relevant agents (eg, NO donors, adenosine receptor agonists, endotoxin derivatives, or opioid receptor agonists), suggesting that this phenomenon might be exploited for therapeutic purposes. The purpose of this review is to summarize current information regarding the pathophysiology and mechanism of late PC. |
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Authors:
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R Bolli |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Circulation research Volume: 87 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2000 Nov |
Date Detail:
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Created Date: 2000-12-01 Completed Date: 2000-12-22 Revised Date: 2005-11-17 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 972-83 Citation Subset: IM |
Affiliation:
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Division of Cardiology, University of Louisville and Jewish Hospital Heart and Lung Institute, Louisville, KY 40292, USA. rbolli@louisville.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine
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metabolism Aldehyde Reductase / metabolism Animals Cyclooxygenase 2 Humans Ischemic Preconditioning* Isoenzymes / metabolism Membrane Proteins Myocardial Ischemia / metabolism*, prevention & control Myocardial Reperfusion* Myocardial Stunning / metabolism*, prevention & control Nitric Oxide / metabolism Nitric Oxide Synthase / metabolism Prostaglandin-Endoperoxide Synthases / metabolism Reactive Oxygen Species / metabolism Receptors, Opioid, delta / metabolism Signal Transduction Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Isoenzymes; 0/Membrane Proteins; 0/Reactive Oxygen Species; 0/Receptors, Opioid, delta; 10102-43-9/Nitric Oxide; 58-61-7/Adenosine; EC 1.1.1.21/Aldehyde Reductase; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/PTGS2 protein, human; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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