2013
Pathophysiological Consequences of TAT-HKII Peptide Administration Are Independent of Impaired Vascular Function and Ensuing Ischemia
Nederlof R, Xie C, Eerbeek O, Koeman A, Milstein DM, Hollmann MW, Mik EG, Warley A, Southworth R, Akar FG, Zuurbier CJ. Pathophysiological Consequences of TAT-HKII Peptide Administration Are Independent of Impaired Vascular Function and Ensuing Ischemia. Circulation Research 2013, 112: e8-e13. PMID: 23329797, PMCID: PMC3596767, DOI: 10.1161/circresaha.112.274308.Peer-Reviewed Original ResearchConceptsVascular functionIschemic preconditioningMyocardial dysfunctionCardiac functionPeptide administrationHexokinase IIOptical action potential mappingAcute myocardial dysfunctionImpaired vascular functionIschemia-reperfusion injuryDeleterious effectsIschemic injuryCardioprotective effectsProtective effectIschemiaPathophysiological consequencesIntact myocardiumDehydrogenase releaseIntact heartAdministrationLactate productionDysfunctionRole of mitochondriaInjuryCritical regulator
2011
Biophysical properties and functional consequences of reactive oxygen species (ROS)‐induced ROS release in intact myocardium
Biary N, Xie C, Kauffman J, Akar FG. Biophysical properties and functional consequences of reactive oxygen species (ROS)‐induced ROS release in intact myocardium. The Journal Of Physiology 2011, 589: 5167-5179. PMID: 21825030, PMCID: PMC3225672, DOI: 10.1113/jphysiol.2011.214239.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntioxidantsArrhythmias, CardiacCyclosporineDiazepamEthidiumFluorescenceFluorescent DyesHydrogen PeroxideIn Vitro TechniquesIntracellular MembranesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardiumOrganometallic CompoundsOxidantsOxidative StressRatsSalicylatesSuperoxidesVoltage-Dependent Anion ChannelsConceptsIncidence of arrhythmiasIntact myocardiumOxidative stressMitochondrial permeability transition poreReactive oxygen speciesSustained ventricular tachycardiaROS releaseExposure of heartsGlobal oxidative stressPerfusion of heartsSuperoxide dismutase/catalase mimetic EUK-134Functional consequencesOS protocolArrhythmia scoreAcute modelDihydroethidium fluorescenceUntreated heartsVentricular tachycardiaVentricular fibrillationOxygen speciesArrhythmic consequencesElevated ROS levelsRat heartEUK-134Perfusion
2002
Unique Topographical Distribution of M Cells Underlies Reentrant Mechanism of Torsade de Pointes in the Long-QT Syndrome
Akar FG, Yan GX, Antzelevitch C, Rosenbaum DS. Unique Topographical Distribution of M Cells Underlies Reentrant Mechanism of Torsade de Pointes in the Long-QT Syndrome. Circulation 2002, 105: 1247-1253. PMID: 11889021, DOI: 10.1161/hc1002.105231.Peer-Reviewed Original ResearchConceptsLong QT syndromeSpecific ion channel mutationsCongenital long QT syndromeM cellsQT interval prolongationIon channel mutationsInterval prolongationReentrant mechanismTdP arrhythmiasConduction blockCanine wedge preparationReentrant circuitTransmural dispersionLeft ventricleAction potentialsTransmural wallIntact myocardiumTopographical distributionChannel mutationsWedge preparationsMidmyocardial cellsRepolarizationLQT2Cellular basisElectrical instability