Glibenclamide attenuates the antiarrhythmic effect of endotoxin with a mechanism not involving KATP channels

İskit, Alper B.; Erkent, Ulkem; Ertunç, Mert; Güç, M. Oğuz; İlhan, Mustafa; Onur, Rüştü

doi:10.1016/j.vph.2006.08.415

Cited by 6 publications

(5 citation statements)

References 36 publications

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“…The prolongation of myocardial action potential duration could be either due to increased Ca 2+ channel activity during the plateau phase or blockade of any of the K + channels. 16 …”

Section: Discussionmentioning

confidence: 99%

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The Effects of Lipopolysaccharide Derivatives in Rodent Models of Cardiac Arrhythmia

Yılmaz¹,

Boz²,

İskit³

2022

The Anatolian Journal of Cardiology

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Background: Several previous studies have suggested that sublethal doses of Escherichia coli lipopolysaccharide (endotoxin) and monophosphoryl lipid A Re595, a non-pyrogenic derivative of Salmonella minnesota lipopolysaccharide, exhibit antiarrhythmic effects in the rat model of ischemia–reperfusion arrhythmias. Methods: In this study, the protective effect of lipopolysaccharide derivatives was also further investigated in drug (aconitine or ouabain)-induced arrhythmia models, and conclusions were drawn with particular emphasis on the molecular characteristics of different types of lipopolysaccharide. Results: The importance of the molecular structure for the antiarrhythmic effect of monophosphoryl lipid A and E. coli lipopolysaccharide was tested in the ischemia–reperfusion arrhythmia model. In contrast to monophosphoryl lipid A from Salmonella typhimurium SL 684 which has only monophosphoryl residue in its structure, monophosphoryl lipid A Re595, obtained from S. minnesota , and E. coli lipopolysaccharide which have both mono and diphosphoryl residue reduced the duration of ventricular tachycardia (e.g., during reperfusion: vehicle: 176 ± 22.8; monophosphoryl lipid A Re595: 132.83 ± 12.1, as second, n = 8-10, P < .05) and the incidence of ventricular fibrillation. The antiarrhythmic effects of E. coli lipopolysaccharide and monophosphoryl lipid A Re595 in ischemia–reperfusion arrhythmia model were absent in either aconitine- (e.g., onset time for ventricular ectopic beats: saline 25.3 5.0, E. coli lipopolysaccharide 24.3 ± 7.1; vehicle: 24.0 ± 4.5, monophosphoryl lipid A SL684 23.8 ± 4.3, as second, n = 6, P > .05) or ouabain-induced arrhythmia models in mice. Conclusion: Therefore, we conclude that lipopolysaccharide derivatives exhibit antiarrhythmic effect only in ischemia–reperfusion arrhythmias, and lipopolysaccharide should possess diphosphoryl groups in its subcomponent composition for this antiarrhythmic effect.

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“…The prolongation of myocardial action potential duration could be either due to increased Ca 2+ channel activity during the plateau phase or blockade of any of the K + channels. 16 …”

Section: Discussionmentioning

confidence: 99%

“…Fundamental surgical procedures used in the present study were described previously by Clark et al 13 and Iskit et al 14 - 16 Briefly, rats (200-300 g) were anesthetized with sodium thiopental (65 mg kg −1 , i.p.) and placed on a heat-insulated-cork sheet-covered operating table.…”

Section: Methodsmentioning

confidence: 99%

The Effects of Lipopolysaccharide Derivatives in Rodent Models of Cardiac Arrhythmia

Yılmaz¹,

Boz²,

İskit³

2022

The Anatolian Journal of Cardiology

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“…Furthermore, we used glibenclamide to investigate if the STS effect is K(ATP)-channeldependent. Glibenclamide is widely and successfully used as a K (ATP)-channel-blocker in the literature (13,(38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

Sodium Thiosulfate Improves Intestinal and Hepatic Microcirculation Without Affecting Mitochondrial Function in Experimental Sepsis

et al. 2021

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IntroductionIn the immunology of sepsis microcirculatory and mitochondrial dysfunction in the gastrointestinal system are important contributors to mortality. Hydrogen sulfide (H2S) optimizes gastrointestinal oxygen supply and mitochondrial respiration predominantly via K(ATP)-channels. Therefore, we tested the hypothesis that sodium thiosulfate (STS), an inducer of endogenous H2S, improves intestinal and hepatic microcirculation and mitochondrial function via K(ATP)-channels in sepsis.MethodsIn 40 male Wistar rats colon ascendens stent peritonitis (CASP) surgery was performed to establish sepsis. Animals were randomized into 4 groups (1: STS 1 g • kg-1 i.p., 2: glibenclamide (GL) 5 mg • kg-1 i.p., 3: STS + GL, 4: vehicle (VE) i.p.). Treatment was given directly after CASP-surgery and 24 hours later. Microcirculatory oxygenation (µHBO2) and flow (µflow) of the colon and the liver were continuously recorded over 90 min using tissue reflectance spectrophotometry. Mitochondrial oxygen consumption in tissue homogenates was determined with respirometry. Statistic: two-way ANOVA + Dunnett´s and Tukey post - hoc test (microcirculation) and Kruskal-Wallis test + Dunn’s multiple comparison test (mitochondria). p < 0.05 was considered significant.ResultsSTS increased µHbO2 (colon: 90 min: + 10.4 ± 18.3%; liver: 90 min: + 5.8 ± 9.1%; p < 0.05 vs. baseline). Furthermore, STS ameliorated µflow (colon: 60 min: + 51.9 ± 71.1 aU; liver: 90 min: + 22.5 ± 20.0 aU; p < 0.05 vs. baseline). In both organs, µHbO2 and µflow were significantly higher after STS compared to VE. The combination of STS and GL increased colonic µHbO2 and µflow (µHbO2 90 min: + 8.7 ± 11.5%; µflow: 90 min: + 41.8 ± 63.3 aU; p < 0.05 vs. baseline), with significantly higher values compared to VE. Liver µHbO2 and µflow did not change after STS and GL. GL alone did not change colonic or hepatic µHbO2 or µflow. Mitochondrial oxygen consumption and macrohemodynamic remained unaltered.ConclusionThe beneficial effect of STS on intestinal and hepatic microcirculatory oxygenation in sepsis seems to be mediated by an increased microcirculatory perfusion and not by mitochondrial respiratory or macrohemodynamic changes. Furthermore, the effect of STS on hepatic but not on intestinal microcirculation seems to be K(ATP)-channel-dependent.

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“…7 This action is mediated by the adenosine-activated potasium acetylcholine (K ACh ) channel effector system. [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] With enhanced adrenergic activity, adenosine attenuates both catecholamineactivated outward I K and inward I Ca , presumably by inhibition of phosphorylation of these channels, because adenosine inhibits adenylate cyclase activity and decrease the generation of cAMP. 7 Adenosine presents antiadrenergic efficiency over delayed rectifier potassium (I K ) and chloride (I Cl ) currents and cAMP-dependent mechanism with L-type Ca þ2 channel current (I CaL ) in both supraventricular and ventricular tissues.…”

Section: Discussionmentioning

confidence: 99%

“…A 2-ms duration and 1-Hz frequency square-wave pulses were delivered from a stimulator (Grass S88, Grass Instruments, Missouri, USA). 8 AP signals were amplified by Axoclamp-2A (Axon Instruments, Foster City, California, USA) and displayed on a digitized oscilloscope (Tektronix, Wilsonville, Oregon, USA). Data were recorded by PowerLab and analyzed by Scope 3.7 software (ADI Instruments, Sydney, Australia).…”

Section: Chemicalsmentioning

confidence: 99%

The role of adenosine receptors on amitriptyline-induced electrophysiological changes on rat atrium

et al. 2012

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We investigated the role of adenosine receptors in amitriptyline-induced cardiac action potential (AP) changes in isolated rat atria. In the first group, APs were recorded after cumulative addition of amitriptyline (1 μM, 10 μM and 50 μM). In other groups, each atrium was incubated with selective adenosine A(1) antagonist (8-cyclopentyl-1,3-dipropylxanthine (DPCPX), 10(-4) M) or selective adenosine A(2a) receptor antagonist (8-(3-chlorostyryl) caffeine, 10(-5) M) before amitriptyline administration. Resting membrane potential, AP amplitude (APA), AP duration at 50% and 80% of repolarization (APD(50) and APD(80), respectively), and the maximum rise and decay slopes of AP were recorded. Amitriptyline (50 μM) prolonged the APD(50) and APD(80) (p < 0.001) and the maximum rise slope of AP was reduced by amitriptyline (p < 0.0001). Amitriptyline reduced maximum decay slope of AP only at 50 μM (p < 0.01). DPCPX significantly decreased the 50-μM amitriptyline-induced APD(50) and APD(80) prolongation (p < 0.001). DPCPX significantly prevented the effects of amitriptyline (1 μM and 50 μM) on maximum rise slope of AP (p < 0.05). DPCPX significantly prevented the amitriptyline-induced (50 μM) reduction in maximum decay slope of AP (p < 0.001). The selective adenosine A(1) receptor antagonist prevented the electrophysiological effects of amitriptyline on atrial AP. A(1) receptor stimulation may be responsible for the cardiovascular toxic effects produced by amitriptyline.

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Glibenclamide attenuates the antiarrhythmic effect of endotoxin with a mechanism not involving KATP channels

Cited by 6 publications

References 36 publications

The Effects of Lipopolysaccharide Derivatives in Rodent Models of Cardiac Arrhythmia

The Effects of Lipopolysaccharide Derivatives in Rodent Models of Cardiac Arrhythmia

Sodium Thiosulfate Improves Intestinal and Hepatic Microcirculation Without Affecting Mitochondrial Function in Experimental Sepsis

The role of adenosine receptors on amitriptyline-induced electrophysiological changes on rat atrium

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