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Article: Bosentan affects 15-F2t-isoprostane adverse effects on postischemic rat hearts

TitleBosentan affects 15-F2t-isoprostane adverse effects on postischemic rat hearts
Authors
Issue Date2011
PublisherElsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsre
Citation
Journal of Surgical Research, 2011, v. 168 n. 1, p. 18-26 How to Cite?
AbstractBACKGROUND: 15-F(2t)-isoprostane (IsoP), a marker of reactive oxygen species-induced oxidative stress, is increased after myocardial ischemia and reperfusion. It exerts deleterious effects on postischemic myocardium accompanied with increased release of endothelin-1 (ET-1), a potent vasoconstrictor. We hypothesized that IsoP exacerbates myocardial ischemia-reperfusion injury by stimulating ET-1 production, and that ET-1 blockade can attenuate or prevent these deleterious effects of IsoP. METHODS: Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit solution (KH) at a constant flow rate of 10 mL/min. Global myocardial ischemia was induced by stopping KH perfusion for 40 min followed by 60 min of reperfusion. Hearts were randomized to one of the five groups (n = 8 each): untreated control, treated with IsoP (100 nM), or the ET-1 receptor A/B antagonist bosentan (1 muM) alone or in combination 10 min prior to, during 40 min global ischemia and 15 min of reperfusion, or treated with IsoP as above plus delayed administration of bosentan after 15 min of reperfusion. RESULTS: Coronary effluent ET-1 concentrations in the IsoP group were higher than those in the control group during ischemia and reperfusion (P < 0.05), which was associated with increased release of cardiac-specific creatine kinase, reduced cardiac contractility during reperfusion, and increased myocardial infarct size (all P < 0.05 versus control). Bosentan administration during early reperfusion exacerbated the IsoP deleterious effects, while delayed administration attenuated it. CONCLUSION: 15-F(2t)-isoprostane-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.
Persistent Identifierhttp://hdl.handle.net/10722/147283
ISSN
2015 Impact Factor: 2.198
2015 SCImago Journal Rankings: 0.928
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China (NSFC)30872446
30872447
University of Hong Kong200801159054
Funding Information:

This study was supported in part by grants 30872446 (to KXL) and 30872447 (to ZX) from the National Natural Science Foundation of China (NSFC), and in part by the Seeding Funding Programme for Basic Research from the University of Hong Kong (URC 200801159054).

References

 

DC FieldValueLanguage
dc.contributor.authorLiu, HMen_US
dc.contributor.authorLiu, KXen_US
dc.contributor.authorCheng, MHen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorLei, Sen_US
dc.contributor.authorIrwin, MGen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-05-29T06:01:13Z-
dc.date.available2012-05-29T06:01:13Z-
dc.date.issued2011en_US
dc.identifier.citationJournal of Surgical Research, 2011, v. 168 n. 1, p. 18-26en_US
dc.identifier.issn0022-4804en_US
dc.identifier.urihttp://hdl.handle.net/10722/147283-
dc.description.abstractBACKGROUND: 15-F(2t)-isoprostane (IsoP), a marker of reactive oxygen species-induced oxidative stress, is increased after myocardial ischemia and reperfusion. It exerts deleterious effects on postischemic myocardium accompanied with increased release of endothelin-1 (ET-1), a potent vasoconstrictor. We hypothesized that IsoP exacerbates myocardial ischemia-reperfusion injury by stimulating ET-1 production, and that ET-1 blockade can attenuate or prevent these deleterious effects of IsoP. METHODS: Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit solution (KH) at a constant flow rate of 10 mL/min. Global myocardial ischemia was induced by stopping KH perfusion for 40 min followed by 60 min of reperfusion. Hearts were randomized to one of the five groups (n = 8 each): untreated control, treated with IsoP (100 nM), or the ET-1 receptor A/B antagonist bosentan (1 muM) alone or in combination 10 min prior to, during 40 min global ischemia and 15 min of reperfusion, or treated with IsoP as above plus delayed administration of bosentan after 15 min of reperfusion. RESULTS: Coronary effluent ET-1 concentrations in the IsoP group were higher than those in the control group during ischemia and reperfusion (P < 0.05), which was associated with increased release of cardiac-specific creatine kinase, reduced cardiac contractility during reperfusion, and increased myocardial infarct size (all P < 0.05 versus control). Bosentan administration during early reperfusion exacerbated the IsoP deleterious effects, while delayed administration attenuated it. CONCLUSION: 15-F(2t)-isoprostane-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.en_US
dc.languageengen_US
dc.publisherElsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsreen_US
dc.relation.ispartofJournal of Surgical Researchen_US
dc.subject.meshCreatine Kinase - metabolismen_US
dc.subject.meshHeart - drug effects - physiopathologyen_US
dc.subject.meshIsoprostanes - pharmacologyen_US
dc.subject.meshMyocardial Reperfusion Injury - metabolism - physiopathologyen_US
dc.subject.meshSulfonamides - pharmacologyen_US
dc.titleBosentan affects 15-F2t-isoprostane adverse effects on postischemic rat heartsen_US
dc.typeArticleen_US
dc.identifier.emailIrwin, MG: mgirwin@hkucc.hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk; zhengyuan_xia@yahoo.comen_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.jss.2009.07.029en_US
dc.identifier.pmid20006348-
dc.identifier.scopuseid_2-s2.0-79955572383en_US
dc.identifier.hkuros162567-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79955572383&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume168en_US
dc.identifier.issue1en_US
dc.identifier.spage18en_US
dc.identifier.epage26en_US
dc.identifier.isiWOS:000290016200024-
dc.publisher.placeUnited Statesen_US
dc.identifier.citeulike5542012-

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