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Conference Paper: Role of the Mitochondrial Permeability Transition Pore in TNF-α -Induced Recovery of Ventricular Contraction and Reduction of Infarct Size in Isolated Rat Hearts Subjected to Ischemia/Reperfusion

TitleRole of the Mitochondrial Permeability Transition Pore in TNF-α -Induced Recovery of Ventricular Contraction and Reduction of Infarct Size in Isolated Rat Hearts Subjected to Ischemia/Reperfusion
Authors
KeywordsTumor necrosis factor-α
heart
ischemiareperfusion
mitochondrial permeability transition pore
Issue Date2004
PublisherIEEE.
Citation
The 26th Annual International Conference of the IEEE Engineering in Medicine and Biology Society Proceedings, San Francisco, CA, USA, 1-5 September 2004, v. 2, p. 3622-3624 How to Cite?
AbstractPretreatment with tumor necrosis factor-α (TNF-α) is known to trigger cardioprotection. TNF-α can activate multiple downstream signaling cascades. However, it is not known whether the mitochondrial permeability transition pore (MitoPTP) is involved in TNF-α -induced cardioprotection. In the present study, we examined whether TNF-α inhibits MitoPTP opening. In isolated rat hearts subjected to 30 min regional ischemia and 120 min reperfusion, pretreatment with 10 U/ml TNF-α for 7 min followed by 10 min washout improved the recovery of left ventricular developed pressure (LVDP) and rate-pressure product (RPP = LVDP × heart rate) during reperfusion and reduced the infarct size. Administration of 20 μ mol/L atractyloside, a MitoPTP opener, for 20 min (last 5 min of ischemia and first 15 min of reperfusion) and pretreatment with 1 μ inhibitor of the Ca2+-activated K+mol/L paxilline, an channel, for 5 min before ischemia, attenuated the recovery of LVDP and RPP and the reduction of infarct size induced by TNF-α. The findings indicate that, in the isolated heart model, TNF-α protects myocardium against ischemia/reperfusion injury via inhibiting MitoPTP opening as well as by activating the Ca2+-activated K+channel.
Persistent Identifierhttp://hdl.handle.net/10722/46971
ISSN

 

DC FieldValueLanguage
dc.contributor.authorGao, Qen_HK
dc.contributor.authorXia, Qen_HK
dc.contributor.authorCao, Cen_HK
dc.contributor.authorZhang, SZen_HK
dc.contributor.authorBruce, ICen_HK
dc.date.accessioned2007-10-30T07:02:45Z-
dc.date.available2007-10-30T07:02:45Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 26th Annual International Conference of the IEEE Engineering in Medicine and Biology Society Proceedings, San Francisco, CA, USA, 1-5 September 2004, v. 2, p. 3622-3624en_HK
dc.identifier.issn1557-170Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/46971-
dc.description.abstractPretreatment with tumor necrosis factor-α (TNF-α) is known to trigger cardioprotection. TNF-α can activate multiple downstream signaling cascades. However, it is not known whether the mitochondrial permeability transition pore (MitoPTP) is involved in TNF-α -induced cardioprotection. In the present study, we examined whether TNF-α inhibits MitoPTP opening. In isolated rat hearts subjected to 30 min regional ischemia and 120 min reperfusion, pretreatment with 10 U/ml TNF-α for 7 min followed by 10 min washout improved the recovery of left ventricular developed pressure (LVDP) and rate-pressure product (RPP = LVDP × heart rate) during reperfusion and reduced the infarct size. Administration of 20 μ mol/L atractyloside, a MitoPTP opener, for 20 min (last 5 min of ischemia and first 15 min of reperfusion) and pretreatment with 1 μ inhibitor of the Ca2+-activated K+mol/L paxilline, an channel, for 5 min before ischemia, attenuated the recovery of LVDP and RPP and the reduction of infarct size induced by TNF-α. The findings indicate that, in the isolated heart model, TNF-α protects myocardium against ischemia/reperfusion injury via inhibiting MitoPTP opening as well as by activating the Ca2+-activated K+channel.en_HK
dc.format.extent700363 bytes-
dc.format.extent555997 bytes-
dc.format.extent3292 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherIEEE.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rights©2004 IEEE. Personal use of this material is permitted. However, permission to reprint/republish this material for advertising or promotional purposes or for creating new collective works for resale or redistribution to servers or lists, or to reuse any copyrighted component of this work in other works must be obtained from the IEEE.en_HK
dc.subjectTumor necrosis factor-αen_HK
dc.subjecthearten_HK
dc.subjectischemiareperfusionen_HK
dc.subjectmitochondrial permeability transition poreen_HK
dc.titleRole of the Mitochondrial Permeability Transition Pore in TNF-α -Induced Recovery of Ventricular Contraction and Reduction of Infarct Size in Isolated Rat Hearts Subjected to Ischemia/Reperfusionen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1557-170X&volume=2&spage=3622&epage=3624&date=2004&atitle=Role+of+the+Mitochondrial+Permeability+Transition+Pore+in+TNF-α+-Induced+Recovery+of+Ventricular+Contraction+and+Reduction+of+Infarct+Size+in+Isolated+Rat+Hearts+Subjected+to+Ischemia/Reperfusionen_HK
dc.description.naturepublished_or_final_versionen_HK

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