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Conference Paper: eNOS and nNOS mediate isoflurane preconditioning

TitleeNOS and nNOS mediate isoflurane preconditioning
Authors
KeywordsBiology
Issue Date2013
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2013 Annual Meeting of Experimental Biology (EB 2013), Boston, MA., 28 March-1 April 2013. In The FASEB Journal, 2013, v. 27 meeting abstracts, no. 920.1 How to Cite?
AbstractAnesthetic preconditioning (APC) has been shown to protect the heart against ischemia and reperfusion injury via a nitric oxide-dependent mechanism. However, the role of nitric oxide synthase (NOS) isoforms in the cardioprotective effect of APC remains elusive. We examined the role of endothelial (eNOS) and neuronal NOS (nNOS) isoforms in cardioprotection by isoflurane. Pentobarbital-anesthetized C57BL/6 and eNOS–/– mice underwent APC or equivalent amounts of air/oxygen (control) prior to 30 min of coronary occlusion followed by 2 h of reperfusion. APC was produced with 1.0 minimum alveolar concentration of the volatile anesthetic isoflurane for 30 min followed by a 15 min washout period. Infarct area and area at risk were delineated by 2,3,5-triphenyltetrazolium chloride and phthalo blue dye, respectively. There were no significant differences in area at risk between groups. APC decreased infarct size in C57BL/6 mice (41±3% vs. 54±3% in control, n=8 mice/group, P<0.05), which was partially blocked by 7-nitroindazole (25 mg/kg), a selective inhibitor for nNOS, administered intraperitoneally 15 min prior to APC. Disruption of eNOS gene did not significantly increase infarct size compared with C57BL/6 mice and partially blocked the cardioprotective effect of APC. Furthermore, APC-elicited decrease in infarct size in eNOS–/– mice was abolished by 7-nitroindazole. Cardiomyocytes were co-cultured with endothelial cells and subsequently exposed to isoflurane (0.5 mM) or air (control) for 60 min prior to 2 h of hypoxia and 2 h of reoxygenation. Isoflurane significantly increased phosphorylated eNOS compared with control. The results demonstrate that eNOS and nNOS synergistically mediate cardioprotection against ischemia and reperfusion injury by isoflurane.
Persistent Identifierhttp://hdl.handle.net/10722/190356
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorGe, ZDen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorWarltier, DCen_US
dc.contributor.authorKersten, JRen_US
dc.date.accessioned2013-09-17T15:20:18Z-
dc.date.available2013-09-17T15:20:18Z-
dc.date.issued2013en_US
dc.identifier.citationThe 2013 Annual Meeting of Experimental Biology (EB 2013), Boston, MA., 28 March-1 April 2013. In The FASEB Journal, 2013, v. 27 meeting abstracts, no. 920.1en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/190356-
dc.description.abstractAnesthetic preconditioning (APC) has been shown to protect the heart against ischemia and reperfusion injury via a nitric oxide-dependent mechanism. However, the role of nitric oxide synthase (NOS) isoforms in the cardioprotective effect of APC remains elusive. We examined the role of endothelial (eNOS) and neuronal NOS (nNOS) isoforms in cardioprotection by isoflurane. Pentobarbital-anesthetized C57BL/6 and eNOS–/– mice underwent APC or equivalent amounts of air/oxygen (control) prior to 30 min of coronary occlusion followed by 2 h of reperfusion. APC was produced with 1.0 minimum alveolar concentration of the volatile anesthetic isoflurane for 30 min followed by a 15 min washout period. Infarct area and area at risk were delineated by 2,3,5-triphenyltetrazolium chloride and phthalo blue dye, respectively. There were no significant differences in area at risk between groups. APC decreased infarct size in C57BL/6 mice (41±3% vs. 54±3% in control, n=8 mice/group, P<0.05), which was partially blocked by 7-nitroindazole (25 mg/kg), a selective inhibitor for nNOS, administered intraperitoneally 15 min prior to APC. Disruption of eNOS gene did not significantly increase infarct size compared with C57BL/6 mice and partially blocked the cardioprotective effect of APC. Furthermore, APC-elicited decrease in infarct size in eNOS–/– mice was abolished by 7-nitroindazole. Cardiomyocytes were co-cultured with endothelial cells and subsequently exposed to isoflurane (0.5 mM) or air (control) for 60 min prior to 2 h of hypoxia and 2 h of reoxygenation. Isoflurane significantly increased phosphorylated eNOS compared with control. The results demonstrate that eNOS and nNOS synergistically mediate cardioprotection against ischemia and reperfusion injury by isoflurane.-
dc.languageengen_US
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_US
dc.subjectBiology-
dc.titleeNOS and nNOS mediate isoflurane preconditioningen_US
dc.typeConference_Paperen_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros221910en_US
dc.identifier.volume27en_US
dc.identifier.issuemeeting abstracts-
dc.publisher.placeUnited States-

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