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
2005
Conduction Abnormalities in Nonischemic Dilated Cardiomyopathy: Basic Mechanisms and Arrhythmic Consequences
Akar FG, Tomaselli GF. Conduction Abnormalities in Nonischemic Dilated Cardiomyopathy: Basic Mechanisms and Arrhythmic Consequences. Trends In Cardiovascular Medicine 2005, 15: 259-264. PMID: 16226681, DOI: 10.1016/j.tcm.2005.08.002.Peer-Reviewed Original ResearchConceptsConduction abnormalitiesVentricular dysfunctionHeart failureMolecular mechanismsLeft ventricular dysfunctionNonischemic heart failureIschemic heart diseaseExtracellular matrixGenesis of arrhythmiasMyocyte excitabilityMechanistic differencesOrgan levelMembrane excitabilityVentricular tachyarrhythmiasDisease etiologyMyocardial infarctionHeart diseaseArrhythmogenic substrateSudden deathArrhythmic consequencesCell couplingAbnormalitiesBasic mechanismsDysfunctionExcitability