| Nitric oxide triggers delayed anesthetic preconditioning-induced cardiac protection via activation of nuclear factor-kappaB and upregulation of inducible nitric oxide synthase. | |
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MedLine Citation:
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PMID: 18708911 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Nitric oxide (NO) plays a pivotal role both in triggering and mediating delayed protection against myocardial I/R injury during anesthetic-induced preconditioning (APC). However, the signaling mechanisms that underlie this phenomenon remain unclear. Using isoflurane as a representative anesthetic, the present study tested the hypothesis that NO released after anesthetic-induced preconditioning initiates delayed cardioprotection via activation of nuclear transcription factor-kappaB (NF-kappaB), leading to myocardial adaptation by upregulation of iNOS and increase in production of NO. Sprague-Dawley rats that received open-chest surgery under pentobarbital anesthesia were subject to 30 min of left coronary artery occlusion, followed by 120 min of reperfusion. Exposure to 60 min of 2.1% isoflurane inhalation with oxygen 24 h before ischemia significantly reduced I/R-induced myocardial infarct size that was associated with overexpression of iNOS protein and increased NO content in the heart. These protective effects were abolished by pretreatment with a NOS inhibitor, N-nitro-L-arginine methyl ester, an NF-kappaB blocker, diethyldithiocarbamate, before isoflurane, or a selective iNOS inhibitor, S-methylisothiourea, before left coronary artery occlusion. Isoflurane exposure also evoked a robust increase in myocardial NO content, followed by nucleus-bound translocation of p65 or p50 subunit of NF-kappaB and increase in NF-kappaB DNA-binding activity in heart tissues. These molecular events after isoflurane exposure were blocked by pretreatment with N-nitro-L-arginine methyl ester. We conclude that NO generated immediately after isoflurane exposure triggers downstream activation of NF-kappaB, resulting in subsequent upregulation of iNOS expression and NO synthesis that mediate APC-induced delayed cardioprotection. |
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Authors:
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Chen Hsiu Chen; Jiin Haur Chuang; Kang Liu; Julie Y H Chan |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Shock (Augusta, Ga.) Volume: 30 ISSN: 1540-0514 ISO Abbreviation: Shock Publication Date: 2008 Sep |
Date Detail:
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Created Date: 2008-08-18 Completed Date: 2008-12-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9421564 Medline TA: Shock Country: United States |
Other Details:
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Languages: eng Pagination: 241-9 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, Republic of China. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Anesthetics, Inhalation
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pharmacology Animals Gene Expression Regulation, Enzymologic Heart / drug effects* Ischemic Preconditioning, Myocardial Isoflurane / pharmacology Male Myocardium / pathology* NF-kappa B / metabolism* Nitric Oxide Synthase Type II / biosynthesis* Protein C / metabolism Rats Rats, Sprague-Dawley Reperfusion Injury Up-Regulation* |
| Chemical | |
Reg. No./Substance:
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0/Anesthetics, Inhalation; 0/NF-kappa B; 0/Protein C; 26675-46-7/Isoflurane; EC 1.14.13.39/Nitric Oxide Synthase Type II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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