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Mitochondrial reactive oxygen species production in excitable cells: modulators of mitochondrial and cell function.Dynamic buffering of mitochondrial Ca2+ during Ca2+ uptake and Na+-induced Ca2+ release.Isoflurane modulates cardiac mitochondrial bioenergetics by selectively attenuating respiratory complexesPotential therapeutic benefits of strategies directed to mitochondria.Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injuryIschemia reperfusion dysfunction changes model-estimated kinetics of myofilament interaction due to inotropic drugs in isolated hearts.Differences in cardiotoxicity of bupivacaine and ropivacaine are the result of physicochemical and stereoselective properties.Reverse electron flow-induced ROS production is attenuated by activation of mitochondrial Ca2+-sensitive K+ channels.Reversible blockade of complex I or inhibition of PKCĪ² reduces activation and mitochondria translocation of p66Shc to preserve cardiac function after ischemiaMitochondrial approaches to protect against cardiac ischemia and reperfusion injury.Differential effects of buffer pH on Ca(2+)-induced ROS emission with inhibited mitochondrial complexes I and III.Adding ROS quenchers to cold K+ cardioplegia reduces superoxide emission during 2-hour global cold cardiac ischemia.Ranolazine reduces Ca2+ overload and oxidative stress and improves mitochondrial integrity to protect against ischemia reperfusion injury in isolated heartsDamage to mitochondrial complex I during cardiac ischemia reperfusion injury is reduced indirectly by anti-anginal drug ranolazine.Reduced mitochondrial Ca2+ loading and improved functional recovery after ischemia-reperfusion injury in old vs. young guinea pig hearts.Cardioprotection with volatile anesthetics: mechanisms and clinical implications.Reactive oxygen species as mediators of cardiac injury and protection: the relevance to anesthesia practice.Protection against cardiac injury by small Ca(2+)-sensitive K(+) channels identified in guinea pig cardiac inner mitochondrial membraneMitochondrial handling of excess Ca2+ is substrate-dependent with implications for reactive oxygen species generation.Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion.Extra-matrix Mg2+ limits Ca2+ uptake and modulates Ca2+ uptake-independent respiration and redox state in cardiac isolated mitochondria.Modulation of mitochondrial bioenergetics in the isolated Guinea pig beating heart by potassium and lidocaine cardioplegia: implications for cardioprotection.Safety and Efficacy of Ranolazine for the Treatment of Chronic Angina Pectoris.Genetically determined mitochondrial preservation and cardioprotection against myocardial ischemia-reperfusion injury in a consomic rat modelComputational analysis of Ca2+ dynamics in isolated cardiac mitochondria predicts two distinct modes of Ca2+ uptake.Human heart conjugate cooling simulation: unsteady thermo-fluid-stress analysis.Isoflurane activates human cardiac mitochondrial adenosine triphosphate-sensitive K+ channels reconstituted in lipid bilayers.Characterization of human cardiac mitochondrial ATP-sensitive potassium channel and its regulation by phorbol ester in vitro.Preconditioning with sevoflurane reduces changes in nicotinamide adenine dinucleotide during ischemia-reperfusion in isolated hearts: reversal by 5-hydroxydecanoic acid.Na+/H+ exchange inhibition with cardioplegia reduces cytosolic [Ca2+] and myocardial damage after cold ischemia.Anesthetic preconditioning: effects on latency to ischemic injury in isolated hearts.How inotropic drugs alter dynamic and static indices of cyclic myoplasmic [Ca2+] to contractility relationships in intact hearts.Cardiotonic drugs differentially alter cytosolic [Ca2+] to left ventricular relationships before and after ischemia in isolated guinea pig hearts.Ischemic preconditioning: triggering role of nitric oxide-derived oxidants in isolated hearts.Effect of low [CaCl2] and high [MgCl2] cardioplegia and moderate hypothermic ischemia on myoplasmic [Ca2+] and cardiac function in intact hearts.Dual exposure to sevoflurane improves anesthetic preconditioning in intact hearts.Anesthetic preconditioning: the role of free radicals in sevoflurane-induced attenuation of mitochondrial electron transport in Guinea pig isolated hearts.Warm ischemic preconditioning improves mitochondrial redox balance during and after mild hypothermic ischemia in guinea pig isolated hearts.Improvement in functional recovery of the isolated guinea pig heart after hyperkalemic reperfusion with adenosine.Improved mitochondrial bioenergetics by anesthetic preconditioning during and after 2 hours of 27 degrees C ischemia in isolated hearts.
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description
onderzoeker
@nl
researcher ORCID ID = 0000-0003-2180-4844
@en
name
David F Stowe
@ast
David F Stowe
@en
David F Stowe
@es
David F Stowe
@nl
type
label
David F Stowe
@ast
David F Stowe
@en
David F Stowe
@es
David F Stowe
@nl
prefLabel
David F Stowe
@ast
David F Stowe
@en
David F Stowe
@es
David F Stowe
@nl
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P1153
7101994483
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P31
P496
0000-0003-2180-4844