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Article: Nitric oxide and protection against cardiac ischemia

TitleNitric oxide and protection against cardiac ischemia
Authors
KeywordsCardiac ischemia
Nitric oxide
Issue Date2011
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cpd/index.htm
Citation
Current Pharmaceutical Design, 2011, v. 17 n. 18, p. 1774-1782 How to Cite?
AbstractNitric oxide (NO) is produced in almost all tissues and it exerts a variety of biological actions under both physiological and pathological conditions. It is synthesized by three distinct enzymes: endothelial (eNOS), neuronal (nNOS) and inducible (iNOS) nitric oxide synthases. NO is a cardioprotective mediator in powerful cardioprotective processes such as pre- and post-conditioning ischemia;they operate largely in a NO-dependent manner. However, the activity of different NOSs isoforms as well as, the bioavailability of NO can be affected by a variety of disease conditions (in particular diabetes) and pathological situations associated with significantly elevated levels of the pro-inflammatory cytokine tumor necrosis factor-αTNF-α). These adversely affect NO-signaling, as well as the efficacy and safety of treatments with NO or NO-containing agents. This brief review focuses on the role of NO in ischemic myocardial protection with emphasis on its contribution to ischemic pre-and post-conditioning cardioprotection. The impact of pathologic conditions on NO bioavailability and NO-signaling and its potential means for improvement, will also be discussed. © 2011 Bentham Science Publishers.
Persistent Identifierhttp://hdl.handle.net/10722/138924
ISSN
2015 Impact Factor: 3.052
2015 SCImago Journal Rankings: 1.220
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, Zen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2011-09-23T05:42:10Z-
dc.date.available2011-09-23T05:42:10Z-
dc.date.issued2011en_HK
dc.identifier.citationCurrent Pharmaceutical Design, 2011, v. 17 n. 18, p. 1774-1782en_HK
dc.identifier.issn1381-6128en_HK
dc.identifier.urihttp://hdl.handle.net/10722/138924-
dc.description.abstractNitric oxide (NO) is produced in almost all tissues and it exerts a variety of biological actions under both physiological and pathological conditions. It is synthesized by three distinct enzymes: endothelial (eNOS), neuronal (nNOS) and inducible (iNOS) nitric oxide synthases. NO is a cardioprotective mediator in powerful cardioprotective processes such as pre- and post-conditioning ischemia;they operate largely in a NO-dependent manner. However, the activity of different NOSs isoforms as well as, the bioavailability of NO can be affected by a variety of disease conditions (in particular diabetes) and pathological situations associated with significantly elevated levels of the pro-inflammatory cytokine tumor necrosis factor-αTNF-α). These adversely affect NO-signaling, as well as the efficacy and safety of treatments with NO or NO-containing agents. This brief review focuses on the role of NO in ischemic myocardial protection with emphasis on its contribution to ischemic pre-and post-conditioning cardioprotection. The impact of pathologic conditions on NO bioavailability and NO-signaling and its potential means for improvement, will also be discussed. © 2011 Bentham Science Publishers.en_HK
dc.languageengen_US
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cpd/index.htmen_HK
dc.relation.ispartofCurrent Pharmaceutical Designen_HK
dc.subjectCardiac ischemiaen_HK
dc.subjectNitric oxideen_HK
dc.titleNitric oxide and protection against cardiac ischemiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1381-6128&volume=17&issue=18&spage=1774&epage=1782&date=2011&atitle=Nitric+oxide+and+protection+against+cardiac+ischemia-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/138161211796391047en_HK
dc.identifier.pmid21631419-
dc.identifier.scopuseid_2-s2.0-79960337132en_HK
dc.identifier.hkuros193354en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79960337132&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue18en_HK
dc.identifier.spage1774en_HK
dc.identifier.epage1782en_HK
dc.identifier.isiWOS:000299621200002-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridXia, Z=7402151748en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike9526383-

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