Effects of Free Radical Production and Scavengers on Occlusion–reperfusion Induced Arrhythmias

Demiryürek, A. Tuncay; Cakici, I; Wainwright, Cherry L.; Wadsworth, R. M.; Kane, Kathleen A.

doi:10.1006/phrs.1998.0391

Cited by 7 publications

(4 citation statements)

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“…TPEN, on the other hand, did exert a significant anti-arrhythmic effect by reducing total arrhythmia count and the incidence of VT during ischaemia. It is unlikely that this was related to the reduction in SOD-1/3 activity since neither superoxide generation nor superoxide scavenging has been associated with a pro- or anti-arrhythmic effect (respectively) in this model ( 53 ) . However, other studies describing the antiarrhythmic effects that TPEN have ascribed these to inhibition of NO accumulation ( 14 ) and activation of the sarcolemmal Na + /Ca 2+ exchanger to prevent Ca 2+ overload ( 15 ) .…”

Section: Discussionmentioning

confidence: 86%

Acute dietary zinc deficiency in rats exacerbates myocardial ischaemia–reperfusion injury through depletion of glutathione

et al. 2019

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Zn plays an important role in maintaining the anti-oxidant status within the heart and helps to counter the acute redox stress that occurs during myocardial ischaemia and reperfusion. Individuals with low Zn levels are at greater risk of developing an acute myocardial infarction; however, the impact of this on the extent of myocardial injury is unknown. The present study aimed to compare the effects of dietary Zn depletion with in vitro removal of Zn (N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN)) on the outcome of acute myocardial infarction and vascular function. Male Sprague–Dawley rats were fed either a Zn-adequate (35 mg Zn/kg diet) or Zn-deficient (<1 mg Zn/kg diet) diet for 2 weeks before heart isolation. Perfused hearts were subjected to a 30 min ischaemia/2 h reperfusion (I/R) protocol, during which time ventricular arrhythmias were recorded and after which infarct size was measured, along with markers of anti-oxidant status. In separate experiments, hearts were challenged with the Zn chelator TPEN (10 µm) before ischaemia onset. Both dietary and TPEN-induced Zn depletion significantly extended infarct size; dietary Zn depletion was associated with reduced total cardiac glutathione (GSH) levels, while TPEN decreased cardiac superoxide dismutase 1 levels. TPEN, but not dietary Zn depletion, also suppressed ventricular arrhythmias and depressed vascular responses to nitric oxide. These findings demonstrate that both modes of Zn depletion worsen the outcome from I/R but through different mechanisms. Dietary Zn deficiency, resulting in reduced cardiac GSH, is the most appropriate model for determining the role of endogenous Zn in I/R injury.

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Section: Discussionmentioning

confidence: 86%

Acute dietary zinc deficiency in rats exacerbates myocardial ischaemia–reperfusion injury through depletion of glutathione

et al. 2019

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“…Another important factor in reperfusion injury is the production of ROS. Administration of ROS scavengers has shown to reduce VF and infarct size in rats and in some cases even ventricular tachycardia and mortality 66,67,71,75,76 . However in all studies drug administration was done before ischemia induction and the application of ROS scavengers in phase II and III trials did not reduce infarct size.…”

Section: Treatment Of Reperfusion Injurymentioning

confidence: 99%

Reperfusion cardiac arrhythmias and their relation to reperfusion induced cell death

Weg

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Reperfusion cardiac arrhythmias and their relation to reperfusion induced cell deathCitation for published version (APA): van der Weg, K. (2018). Reperfusion cardiac arrhythmias and their relation to reperfusion induced cell death. Proefschriftmaken.nl II Uitgeverij Boxpress. https://doi.org/10.Design by: Bregje Jaspers, ProefschriftOntwerp.nl Printed by: ProefschriftMaken, www.proefschriftmaken.nl © Kirian van der Weg Reperfusion cardiac arrhythmias and their relation to reperfusion induced cell death PROEFSCHRIFT ter verkrijging van de graad van doctor aan de Universiteit Maastricht, op gezag van Rector Magnificius, Prof. dr. Rianne M. Letschert, volgens het besluit van het college van Decanen, in het openbaar te verdedigen op vrijdag 21 december 2018 om 12.00 uur door Kirian van der Weg

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“…Administration of ROS scavengers has been shown to reduce ventricular fibrillation and infarct size in rats and in some cases even ventricular tachycardia and mortality. 66,67,71,75,76 However, in all studies drug administration was carried out before ischaemia induction and the application of ROS scavengers in phase II and III trials did not reduce infarct size.…”

Section: Treatment Of Reperfusion Injurymentioning

confidence: 99%

Editor’s Choice- Reperfusion cardiac arrhythmias and their relation to reperfusion-induced cell death

Weg

Prinzen

Gorgels

2018

European Heart Journal: Acute Cardiovascular Care

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Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.

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Effects of Free Radical Production and Scavengers on Occlusion–reperfusion Induced Arrhythmias

Cited by 7 publications

References 0 publications

Acute dietary zinc deficiency in rats exacerbates myocardial ischaemia–reperfusion injury through depletion of glutathione

Acute dietary zinc deficiency in rats exacerbates myocardial ischaemia–reperfusion injury through depletion of glutathione

Reperfusion cardiac arrhythmias and their relation to reperfusion induced cell death

Editor’s Choice- Reperfusion cardiac arrhythmias and their relation to reperfusion-induced cell death

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