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Conference Paper: Endothelin-1 blockade with bosentan attenuates15-F2t-Isoprostane adverse effects on postischemic rat hearts

TitleEndothelin-1 blockade with bosentan attenuates15-F2t-Isoprostane adverse effects on postischemic rat hearts
Authors
KeywordsBiology
Issue Date2010
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental Biology Annual Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24, Meeting abstract suppl., abstract no. 573.3 How to Cite?
Abstract15-F2t-Isoprostane (IsoP), a specific marker of oxidative stress, is increased after myocardial ischemia. It exerts deleterious effects on postischemic myocardium. We hypothesized that IsoP exacerbates post-ischemic myocardial injury by stimulating endothelin-1 (ET-1) production. Adult rat hearts were perfused by the Langendorff technique. Global myocardial ischemia was induced by stopping perfusion for 40 min followed by 60 min of reperfusion. Hearts were randomized to one of five groups: untreated (C), treated with IsoP (100 nM) or the ET-1 receptor A/B antagonist bosentan (1 µM) alone or in combination 10 min prior to ischemia and for 15 min during reperfusion or treated with IsoP as above plus delayed bosentan administration 15 min after reperfusion. Coronary effluent ET-1 levels in the IsoP group were higher than those in the C group during reperfusion accompanied with increased release of cardiac-specific creatine kinase, reduced cardiac contractility and increased myocardial infarct size (all p<0.05 vs. C). Bosentan administration during early reperfusion exacerbated the IsoP deleterious effects while delayed administration attenuated it. It is concluded that IsoP-induced ET-1 production during later reperfusion is detrimental to functional recovery of damaged myocardium while ET-1 increase during early reperfusion seems to improve it.
DescriptionOpen Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/126893
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorXia, Zen_HK
dc.contributor.authorLiu, HMen_HK
dc.contributor.authorXia, ZYen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorLei, Sen_HK
dc.contributor.authorMao, Xen_HK
dc.contributor.authorIrwin, MGen_HK
dc.date.accessioned2010-10-31T12:54:40Z-
dc.date.available2010-10-31T12:54:40Z-
dc.date.issued2010en_HK
dc.identifier.citationExperimental Biology Annual Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24, Meeting abstract suppl., abstract no. 573.3en_HK
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/126893-
dc.descriptionOpen Access Journal-
dc.description.abstract15-F2t-Isoprostane (IsoP), a specific marker of oxidative stress, is increased after myocardial ischemia. It exerts deleterious effects on postischemic myocardium. We hypothesized that IsoP exacerbates post-ischemic myocardial injury by stimulating endothelin-1 (ET-1) production. Adult rat hearts were perfused by the Langendorff technique. Global myocardial ischemia was induced by stopping perfusion for 40 min followed by 60 min of reperfusion. Hearts were randomized to one of five groups: untreated (C), treated with IsoP (100 nM) or the ET-1 receptor A/B antagonist bosentan (1 µM) alone or in combination 10 min prior to ischemia and for 15 min during reperfusion or treated with IsoP as above plus delayed bosentan administration 15 min after reperfusion. Coronary effluent ET-1 levels in the IsoP group were higher than those in the C group during reperfusion accompanied with increased release of cardiac-specific creatine kinase, reduced cardiac contractility and increased myocardial infarct size (all p<0.05 vs. C). Bosentan administration during early reperfusion exacerbated the IsoP deleterious effects while delayed administration attenuated it. It is concluded that IsoP-induced ET-1 production during later reperfusion is detrimental to functional recovery of damaged myocardium while ET-1 increase during early reperfusion seems to improve it.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_HK
dc.subjectBiology-
dc.titleEndothelin-1 blockade with bosentan attenuates15-F2t-Isoprostane adverse effects on postischemic rat heartsen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=24, Meeting Abstract Suppl. 573.3 &spage=573.3&epage=&date=2010&atitle=Endothelin-1+blockade+with+bosentan+attenuates15-F2t-Isoprostane+adverse+effects+on+postischemic+rat+hearts-
dc.identifier.emailXia, Z: zhengyuan_xia@yahoo.comen_HK
dc.identifier.emailLiu, HM: huimin_liu2006@126.comen_HK
dc.identifier.emailLei, S: leishaoqing@163.comen_HK
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros171207en_HK
dc.identifier.volume24en_HK
dc.identifier.issueMeeting abstract suppl.-
dc.description.otherExperimental Biology Annual Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24, Meeting abstract suppl., abstract no. 573.3-

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