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Article: Molecular basis of electrocardiographic ST-segment elevation

TitleMolecular basis of electrocardiographic ST-segment elevation
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2000
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 2000, v. 87 n. 10, p. 837-839 How to Cite?
AbstractST elevation is a classical hallmark of acute transmural myocardial ischemia. Indeed, ST elevation is the major clinical criterion for committing patients with chest pain to emergent coronary revascularization. Despite its clinical importance, the mechanism of ST elevation remains unclear. Various studies have suggested that activation of sarcolemmal ATP-sensitive potassium (K(ATP)) channels by ischemic ATP depletion may play a role, but little direct evidence is available. We studied mice with homozygous knockout (KO) of the Kir6.2 gene, which encodes the pore-forming subunit of cardiac surface K(ATP) channels. Patch-clamp studies in cardiomyocytes confirmed that surface K(ATP) current was indeed absent in KO, but robust in cells from wild-type mice (WT). We then measured continuous electrocardiograms in anesthetized adult mice before and after open-chest ligation of the left anterior descending artery (LAD). Whereas ST elevation was readily evident in WT after LAD ligation, it was markedly suppressed in KO. Such qualitative differences persisted for the rest of the 60-minute observation period of ischemia. In support of the concept that K(ATP) channels are responsible for ST elevation, the surface K(ATP) channel blocker HMR1098 (5 mg/kg IP) suppressed early ST elevation in WT. Thus, the opening of sarcolemmal K(ATP) channels underlies ST elevation during ischemia. These data are the first to link a specific gene product with a common electrocardiographic phenomenon.
Persistent Identifierhttp://hdl.handle.net/10722/91519
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, RAen_HK
dc.contributor.authorLeppo, Men_HK
dc.contributor.authorMiki, Ten_HK
dc.contributor.authorSeino, Sen_HK
dc.contributor.authorMarbán, Een_HK
dc.date.accessioned2010-09-17T10:20:43Z-
dc.date.available2010-09-17T10:20:43Z-
dc.date.issued2000en_HK
dc.identifier.citationCirculation Research, 2000, v. 87 n. 10, p. 837-839en_HK
dc.identifier.issn0009-7330en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91519-
dc.description.abstractST elevation is a classical hallmark of acute transmural myocardial ischemia. Indeed, ST elevation is the major clinical criterion for committing patients with chest pain to emergent coronary revascularization. Despite its clinical importance, the mechanism of ST elevation remains unclear. Various studies have suggested that activation of sarcolemmal ATP-sensitive potassium (K(ATP)) channels by ischemic ATP depletion may play a role, but little direct evidence is available. We studied mice with homozygous knockout (KO) of the Kir6.2 gene, which encodes the pore-forming subunit of cardiac surface K(ATP) channels. Patch-clamp studies in cardiomyocytes confirmed that surface K(ATP) current was indeed absent in KO, but robust in cells from wild-type mice (WT). We then measured continuous electrocardiograms in anesthetized adult mice before and after open-chest ligation of the left anterior descending artery (LAD). Whereas ST elevation was readily evident in WT after LAD ligation, it was markedly suppressed in KO. Such qualitative differences persisted for the rest of the 60-minute observation period of ischemia. In support of the concept that K(ATP) channels are responsible for ST elevation, the surface K(ATP) channel blocker HMR1098 (5 mg/kg IP) suppressed early ST elevation in WT. Thus, the opening of sarcolemmal K(ATP) channels underlies ST elevation during ischemia. These data are the first to link a specific gene product with a common electrocardiographic phenomenon.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_HK
dc.relation.ispartofCirculation Researchen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.subject.meshAdenosine Triphosphate - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBenzamides - pharmacologyen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshElectrocardiographyen_HK
dc.subject.meshHeart Conduction System - drug effects - metabolism - physiopathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshMyocardial Ischemia - etiology - metabolism - physiopathologyen_HK
dc.subject.meshPatch-Clamp Techniquesen_HK
dc.subject.meshPotassium - metabolismen_HK
dc.subject.meshPotassium Channel Blockersen_HK
dc.subject.meshPotassium Channels - deficiency - genetics - metabolismen_HK
dc.subject.meshPotassium Channels, Inwardly Rectifyingen_HK
dc.subject.meshSarcolemma - metabolismen_HK
dc.titleMolecular basis of electrocardiographic ST-segment elevationen_HK
dc.typeArticleen_HK
dc.identifier.emailLi, RA:ronaldli@hkucc.hku.hken_HK
dc.identifier.authorityLi, RA=rp01352en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid11073877-
dc.identifier.scopuseid_2-s2.0-0034634291en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034634291&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume87en_HK
dc.identifier.issue10en_HK
dc.identifier.spage837en_HK
dc.identifier.epage839en_HK
dc.identifier.isiWOS:000165513000004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, RA=7404724466en_HK
dc.identifier.scopusauthoridLeppo, M=6602511910en_HK
dc.identifier.scopusauthoridMiki, T=7401680016en_HK
dc.identifier.scopusauthoridSeino, S=23390248600en_HK
dc.identifier.scopusauthoridMarbán, E=8075977300en_HK

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