Effects of glyburide on ischemia-induced changes in extracellular potassium and local myocardial activation: A potential new approach to the management of ischemia-induced malignant ventricular arrhythmias

Bekheit, S; Restivo, Mark; Boutjdir, Mohamed; Henkin, Raphael; Gooyandeh, Kaveh; Assadi, Mahshid A.; Khatib, Said Y.; Gough, William B.; El‐Sherif, Nabil

doi:10.1016/s0002-8703(05)80231-5

Cited by 77 publications

(19 citation statements)

References 29 publications

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“…A number of investigators have shown that glibenclamide prevents effects related to ischemia (3,17,56,60). In all of these reports, glibenclamide shows clear effects, although relatively high concentrations were needed (3-300 M) and often only partial restoration was achieved.…”

Section: Drugs and Solutionsmentioning

confidence: 99%

Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K⁺ channels in rat hearts

Cuong

Kim²,

Youm³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Nitric oxidecGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K ϩ channels in rat hearts. Am J Physiol Heart Circ Physiol 290: H1808 -H1817, 2006. First published December 9, 2005 doi:10.1152/ajpheart.00772.2005.-Nitric oxide (NO) plays an important role in anoxic preconditioning to protect the heart against ischemia-reperfusion injuries. The present work was performed to study better the NO-cGMP-protein kinase G (PKG) signaling pathway in the activation of both sarcolemmal and mitochondrial ATP-sensitive K ϩ (KATP) channels during anoxic preconditioning (APC) and final influence on reducing anoxia-reperfusion (A/R)-induced cardiac damage in rat hearts. The upstream regulating elements controlling NO-cGMP-PKG signal-induced KATP channel opening that leads to cardioprotection were investigated. The involvement of both inducible and endothelial NO synthases (iNOS and eNOS) in the progression of this signaling pathway was followed. Final cellular outcomes of ischemia-induced injury after different preconditioning in the form of lactate dehydrogenase release, DNA strand breaks, and malondialdehyde formation as indexes of cell injury and lipid peroxidation, respectively, were investigated. The lactate dehydrogenase and malondialdehyde values decreased in the groups that underwent preconditioning periods with specific mitochondrial KATP channels opener diazoxide (100 M), nonspecific mitochondrial KATP channels opener pinacidil (50 M), S-nitroso-Nacetylpenicillamine (SNAP, 300 M), or ␤-phenyl-1,N 2 -etheno-8-bromoguanosine-3Ј,5Ј-cyclicmonophosphorothioate, Sp-isomer (10 M) before the A/R period. Preconditioning with SNAP significantly reduced the DNA damage. The effect was blocked by glibenclamide (50 M), 5-hydroxydecanoate (100 M), N G -nitro-L-arginine methyl ester (200 M), and ␤-phenyl-1,N 2 -etheno-8-bromoguanosine-3Ј,5Ј-cyclic monophosphorothioate, Rp-isomer (1 M). The results suggest iNOS, rather than eNOS, as the major contributing NO synthase during APC treatment. Moreover, the PKG shows priority over NO as the upstream regulator of NO-cGMP-PKG signal-induced KATP channel opening that leads to cardioprotection during APC treatment.guanosine 3Ј,5Ј-cyclic monophosphate; adenosine 5Ј-triphosphate; oxidative damage ISCHEMIC PRECONDITIONING, in which short-term occlusion and reperfusion of a coronary artery are followed by long-term occlusion, can reduce subsequent ischemia-induced injury to the heart (42). Nitric oxide (NO), protein kinase G (PKG), and ATP-sensitive K ϩ (K ATP ) channels (both the sarcolemmal and mitochondrial subtypes) can mimic the effects of ischemic preconditioning in the heart, and mitochondrial K ATP channels appear to be the end effectors (19,20,25). The activation of these channels may improve the recovery of regional contractility of myocardium by shortening the duration of action potentials and by attenuating membrane depolarization, both of which would decrease myocardial contractility and reduce energy expenditure during ischem...

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Section: Drugs and Solutionsmentioning

confidence: 99%

Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K⁺ channels in rat hearts

Cuong

Kim²,

Youm³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Tissue trauma causes the cells to release potassium into the extracellular fluid, producing hyperkalemia. The ischemic myocardium may release potassium into the extracellular space, which can cause regional hyperkalemia and extracellular potassium accumulation in the ischemic heart [5,6,7,8,9,10,11,12]. There is evidence showing that extracellular potassium [K + ] e begins to rise within 30 s of acute ligation of coronary artery, reaching a value of approximately 11 m M after 8 min [5].…”

Section: Introductionmentioning

confidence: 99%

“…The influence of high extracellular potassium on the effect of anti-arrhythmic drugs on HERG channel was evaluated by increasing [K + ] e from 5 to 10 mmol/l. Levels as high [K + ] e as 10 mmol/l is not often found in the plasma of hyperkalemic patient, but this level of [K + ] e is readily achieved in cardiac ischemic regions [5,6,7,8,9,10,11,12] and has been used in previous studies examining the effect of hyperkalemia on anti-arrhythmic drugs [15, 16, 19]. Five IKr-blocking anti-arrhythmic drugs, amiodarone, azimilide, dofetilide, quinidine and racemate sotalol, were studied to determine their effect on IKr at normal and increased extracellular potassium concentrations.…”

Section: Introductionmentioning

confidence: 99%

The Effect of High Extracellular Potassium on IKr Inhibition by Anti-Arrhythmic Agents

Lin

Ke²,

Cvetanovic³

et al. 2006

Cardiology

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Background: Hyperkalemia is a potentially life-threatening disorder frequently occurring in hospitalized patients. The ischemic myocardium releases potassium into the extracellular space which can cause regional hyperkalemia. These changes may modify the effects of anti-arrhythmic drugs acting on the rapid component of the delayed rectifier potassium current (IKr). We evaluated the influence of increased extracellular potassium concentration [K⁺]_e on IKr inhibition by amiodarone, azimilide, dofetilide, quinidine and sotalol. Methods and Results: Experiments were performed at room temperature. IKr current was studied by using HERG gene expressed in Xenopus oocytes as a model of cardiac IKr. Two-electrode voltage clamp technique was employed. The recording bath solutions contained either 5 or 10 mmol/l KCl. Amiodarone, azimilide, dofetilide, quinidine and sotalol all produced a dose-dependent inhibition of HERG current. At 5 mmol/l [K⁺]_e, the IC₅₀ was 37.0 ± 12.5 µM for amiodarone, 5.8 ± 0.4 µM for azimilide, 1.5 ± 0. 2 µM for dofetilide, 9.1 ± 1.5 µM for quinidine, and 5.1 ± 0.8 mM for sotalol. Raising the extracellular potassium to 10 mmol/l, HERG block by azimilide, dofetilide, quinidine and sotalol was significantly decreased, while the block by amiodarone was unchanged. The differences in the percentage current block produced by 3 µM drugs at 5 and 10 mmol/l [K⁺]_e were: –0.9% for amiodarone, 13.8% for quinidine, 20.5% for azimilide, and 16.2% for dofetilide. The differences in percentage block between 5 and 10 mmol/l [K⁺]_e by sotalol 10 and 30 mM were 7.1 and 5.6%. At 10 mmol/l [K⁺]_e, the IC₅₀ was increased for azimilide, dofetilide, quinidine and sotalol but not for amiodarone; the IC₅₀ was 24.7 ± 7.4 µM for amiodarone, 29.3 ± 3.9 µM for azimilide, 2.7 ± 0.2 µM for dofetilide, 27.6 ± 4.0 µM for quinidine, and 7.2 ± 1.7 mM for sotalol. Conclusion: Inhibition of IKr by azimilide, quinidine, dofetilide and sotalol was diminished by increasing [K⁺]_e, while the inhibition by amiodarone was unchanged at normal and high [K⁺]_e. The differential effects of azimilide, dofetilide, quinidine and sotalol at normal and high [K⁺]_e could be pro-arrhythmic by favoring re-entry arrhythmias. These results further support the unique electrophysiological effect of amiodarone.

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“…The increase in [K + ] e during ischemia has been attributed to enhancement of K + conductance via ATP-sensitive K + channels [14][15][16][17] , anion-coupled K + loss 18) , activation of Na + -activated or arachidonic acid-activated K + channels 19) , suppression of the Na + pump 20) , and shrinkage of the extracellular space 21) . We have shown that the increase in [K + ] e is due to multiple factors, including K conductance across the cell membrane channels, K driving force which is reflected by the amount of time at which the action potential is at its plateau voltage, and the metabolic effects of ischemia on the cell membrane 22) .…”

Section: Discussionmentioning

confidence: 99%

“…The rise in [K + ] e has been attributed to enhancement of K + conductance via ATP-sensitive K + channels [14][15][16][17] , anion-coupled K + loss 18) , activation of Na + -activated or arachidonic acid-activated K + channels 19) , suppression of the Na + pump 20) , and shrinkage of extracellular space 21) . Intracellular pH (pH i ) decreases as protons are produced during hydrolysis of adenosine triphosphate (ATP) and accumulate during production of lactic acid.…”

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confidence: 99%

Contribution of Mechanical Activity to Extracellular K<sup>+</sup> and H<sup>+</sup> Accumulation in Ischemic Porcine Heart

Watanabe

Gettes

2017

Nichidai Igaku Zasshi

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+-and pH-sensitive electrodes and a pair of ultrasonic crystals into the mid-myocardium. We also placed a floating microelectrode in the subepicardium of the ischemic zone. The carotid artery was shunted to the LAD through a roller pump, and BDM (10 mM, n = 7) or pinacidil (50 μM, n = 8) was infused to the LAD shunt in advance of no-flow ischemia. Regional systolic shortening became dyskinetic with the BDM infusion and decreased from 20.1 ± 1.6% to 4.9 ± 1.6% with pinacidil. APD was not affected by BDM, but it decreased from 348 ± 14 ms to 206 ± 14 ms (P < 0.001) with the infusion of pinacidil prior to ischemia. Both pinacidil and BDM attenuated the rise in [K + ] e , but the effect of pinacidil was greater. Both agents reduced the fall in pHe, but this effect was greater with BDM. Pinacidil-induced APD shortening was maintained during ischemia; BDM did not affect APD shortening during ischemia. The fall in pHe during ischemia appears to be related mainly to mechanical activity but the corresponding increase in [K + ] e is more attributable to APD.

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Effects of glyburide on ischemia-induced changes in extracellular potassium and local myocardial activation: A potential new approach to the management of ischemia-induced malignant ventricular arrhythmias

Cited by 77 publications

References 29 publications

Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K⁺ channels in rat hearts

Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K⁺ channels in rat hearts

The Effect of High Extracellular Potassium on IKr Inhibition by Anti-Arrhythmic Agents

Contribution of Mechanical Activity to Extracellular K<sup>+</sup> and H<sup>+</sup> Accumulation in Ischemic Porcine Heart

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Effects of glyburide on ischemia-induced changes in extracellular potassium and local myocardial activation: A potential new approach to the management of ischemia-induced malignant ventricular arrhythmias

Cited by 77 publications

References 29 publications

Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K+ channels in rat hearts

Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K+ channels in rat hearts

The Effect of High Extracellular Potassium on IKr Inhibition by Anti-Arrhythmic Agents

Contribution of Mechanical Activity to Extracellular K<sup>+</sup> and H<sup>+</sup> Accumulation in Ischemic Porcine Heart

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Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K⁺ channels in rat hearts

Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K⁺ channels in rat hearts