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Article: Postconditioning attenuates myocardial injury by reducing nitro-oxidative stress in vivo in rats and in humans

TitlePostconditioning attenuates myocardial injury by reducing nitro-oxidative stress in vivo in rats and in humans
Authors
KeywordsInducible NO synthase (iNOS)
Myocardial ischaemia/reperfusion
Peroxynitrite
Postconditioning
Issue Date2011
PublisherPortland Press Ltd. The Journal's web site is located at http://www.clinsci.org/
Citation
Clinical Science, 2011, v. 120 n. 6, p. 251-261 How to Cite?
AbstractIn the present study, we hypothesized that postcon (postconditioning) confers cardioprotection in vivo by reducing the production of ONOO - (peroxynitrite) and nitro-oxidative stress subsequent to the inhibition of the iNOS (inducible NO synthase). Patients with AMI (acute myocardial infarct) were randomly assigned to undergo percutaneous coronary intervention without (control) or with ischaemic postcon by three episodes of 30-s inflation and 30-s deflation of the angioplasty balloon. Animal models of MI/R (myocardial ischaemia/reperfusion) injury were induced in rats by occluding the left coronary artery for 40 min followed by 4-h reperfusion. Rats were randomized to receive vehicle, postcon (three cycles of 10-s reperfusion and 10-s coronary re-occlusion preceding full reperfusion), the selective iNOS inhibitor 1400W or postcon plus 3-morpholinosydnonimine (an ONOO - donor). Postcon in patients reduced iNOS activity in white blood cells, decreased plasma nitrotyrosine, a fingerprint of ONOO - and an index of nitro-oxidative stress, and improved cardiac function (P<0.01 compared with control). In rats, postcon reduced post-ischaemic myocardial iNOS activity and nitrotyrosine formation, reduced myocardial infarct size (all P<0.05 compared with control) and improved cardiac function. Administration of 1400W resembled, whereas 3-morpholinosydnonimine abolished, the effects of postcon. In conclusion, reduction in ONOO - -induced nitro-oxidative stress subsequent to the inhibition of iNOS represents a major mechanism whereby postcon confers cardioprotection in vivo. © The Authors Journal compilation © 2011 Biochemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/142297
ISSN
2015 Impact Factor: 4.996
2015 SCImago Journal Rankings: 2.427
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Sciences Foundation of China (NSFC)30800448
30770875
Research Grants Council of Hong Kong782910
Funding Information:

This study was supported, in part, by the National Natural Sciences Foundation of China (NSFC) [grant numbers 30800448 (to Q.F.), 30770875 (to X.-C.Y.)]; and the Research Grants Council of Hong Kong General Research Fund [grant number 782910 M (to Z.X.)].

References

 

DC FieldValueLanguage
dc.contributor.authorFan, Qen_HK
dc.contributor.authorYang, XCen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorWang, LFen_HK
dc.contributor.authorLiu, SHen_HK
dc.contributor.authorGe, YGen_HK
dc.contributor.authorChen, MLen_HK
dc.contributor.authorWang, Wen_HK
dc.contributor.authorZhang, LKen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorXia, Zen_HK
dc.date.accessioned2011-10-28T02:42:22Z-
dc.date.available2011-10-28T02:42:22Z-
dc.date.issued2011en_HK
dc.identifier.citationClinical Science, 2011, v. 120 n. 6, p. 251-261en_HK
dc.identifier.issn0143-5221en_HK
dc.identifier.urihttp://hdl.handle.net/10722/142297-
dc.description.abstractIn the present study, we hypothesized that postcon (postconditioning) confers cardioprotection in vivo by reducing the production of ONOO - (peroxynitrite) and nitro-oxidative stress subsequent to the inhibition of the iNOS (inducible NO synthase). Patients with AMI (acute myocardial infarct) were randomly assigned to undergo percutaneous coronary intervention without (control) or with ischaemic postcon by three episodes of 30-s inflation and 30-s deflation of the angioplasty balloon. Animal models of MI/R (myocardial ischaemia/reperfusion) injury were induced in rats by occluding the left coronary artery for 40 min followed by 4-h reperfusion. Rats were randomized to receive vehicle, postcon (three cycles of 10-s reperfusion and 10-s coronary re-occlusion preceding full reperfusion), the selective iNOS inhibitor 1400W or postcon plus 3-morpholinosydnonimine (an ONOO - donor). Postcon in patients reduced iNOS activity in white blood cells, decreased plasma nitrotyrosine, a fingerprint of ONOO - and an index of nitro-oxidative stress, and improved cardiac function (P<0.01 compared with control). In rats, postcon reduced post-ischaemic myocardial iNOS activity and nitrotyrosine formation, reduced myocardial infarct size (all P<0.05 compared with control) and improved cardiac function. Administration of 1400W resembled, whereas 3-morpholinosydnonimine abolished, the effects of postcon. In conclusion, reduction in ONOO - -induced nitro-oxidative stress subsequent to the inhibition of iNOS represents a major mechanism whereby postcon confers cardioprotection in vivo. © The Authors Journal compilation © 2011 Biochemical Society.en_HK
dc.languageengen_US
dc.publisherPortland Press Ltd. The Journal's web site is located at http://www.clinsci.org/en_HK
dc.relation.ispartofClinical Scienceen_HK
dc.rightsThe final version of record is available at [http://www.clinsci.org/].-
dc.subjectInducible NO synthase (iNOS)en_HK
dc.subjectMyocardial ischaemia/reperfusionen_HK
dc.subjectPeroxynitriteen_HK
dc.subjectPostconditioningen_HK
dc.subject.meshAngioplasty, Balloon, Coronary - methods-
dc.subject.meshDisease Models, Animal-
dc.subject.meshEnzyme Inhibitors - therapeutic use-
dc.subject.meshIschemic Postconditioning - methods-
dc.subject.meshMyocardial Reperfusion Injury - physiopathology - prevention and control-
dc.titlePostconditioning attenuates myocardial injury by reducing nitro-oxidative stress in vivo in rats and in humansen_HK
dc.typeArticleen_HK
dc.identifier.emailIrwin, MG:mgirwin@hku.hken_HK
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1042/CS20100369en_HK
dc.identifier.pmid20919993-
dc.identifier.scopuseid_2-s2.0-79251633484en_HK
dc.identifier.hkuros184502en_US
dc.identifier.hkuros203036-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79251633484&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume120en_HK
dc.identifier.issue6en_HK
dc.identifier.spage251en_HK
dc.identifier.epage261en_HK
dc.identifier.eissn1470-8736-
dc.identifier.isiWOS:000288479300009-
dc.publisher.placeUnited Kingdomen_HK

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