The Effect of Acute Versus Delayed Remote Ischemic Preconditioning on Reperfusion Induced Ventricular Arrhythmias

Dow, B S Joan; Bhandari, Anil K.; Simkhovich, Boris Z.; Hale, L B S Sharon; Kloner, Robert A.

doi:10.1111/j.1540-8167.2012.02397.x

Cited by 28 publications

(21 citation statements)

References 42 publications

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“…Different authors have evaluated the possible intracellular mechanisms involved in the rIPC pathway. However, most of these studies have investigated mechanisms at time points that are different from the ones used in the present study [during early reperfusion or in late reperfusion (Dow et al 2012)] and also using different animal species (Konstantinov et al 2005;Donato et al 2013;Brandenburger et al 2014), making difficult to establish a comparison. In agreement with our findings, Li et al (2010) showed that rIPC induces activation of Phosphatidylinositol 3-kinase and inhibition of Glycogen synthase kinase before myocardial ischaemia.…”

Section: Discussionmentioning

confidence: 97%

Myocardial triggers involved in activation of remote ischaemic preconditioning

Donato

Goyeneche

Garcés

et al. 2016

Experimental Physiology

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New Findings r What is the central question of this study?Ischaemia-reperfusion of peripheral tissues protects the heart from subsequent myocardial ischaemia-reperfusion injury, a phenomenon referred to as remote ischaemic preconditioning (rIPC). This study evaluated the possible myocardial triggers of rIPC. r What is the main finding and its importance?Remote ischaemic preconditioning reduces infarct size through a vagal pathway and a mechanism involving phosphorylation of Akt and endothelial nitric oxide synthase, opening of mitochondrial ATP-dependent K + channels and an increase in mitochondrial H 2 O 2 production. All these phenomena occur before the myocardial ischaemia; hence, they could act as 'triggers' of rIPC.It has been proposed that remote ischaemic preconditioning (rIPC) activates a parasympathetic neural pathway. However, the myocardial intracellular mechanism of rIPC remains unclear. Here, we characterized some of the intracellular signals participating as rIPC triggers. Isolated rat hearts were subjected to 30 min of global ischaemia and 120 min of reperfusion (Non-rIPC group). In a second group, before the isolation of the heart, an rIPC protocol (three cycles of hindlimb ischaemia-reperfusion) was performed. The infarct size was measured with tetrazolium staining. Expression/phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) and mitochondrial H 2 O 2 production were evaluated at the end of the rIPC protocol, before myocardial ischaemia-reperfusion. The rIPC significantly decreased the infarct size and induced Akt and eNOS phosphorylation. The protective effect on infarct size was abolished by cervical vagal section, l-NAME (an NO synthesis inhibitor) and 5-hydroxydecanoate

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Section: Discussionmentioning

confidence: 97%

Myocardial triggers involved in activation of remote ischaemic preconditioning

Donato

Goyeneche

Garcés

et al. 2016

Experimental Physiology

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“…; Dow et al . ), very little is known about the effect of RIPC on the incidence and severity of ischaemic tachyarrhythmias.…”

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confidence: 99%

“…In this regard, it seems worthwhile to perform additional experimental studies on RIPC, particularly those aimed at the investigation of RIPC protocols and end-points. For instance, while it is well established that RIPC results in infarct size limitation (Gho et al 1996;Birnbaum et al 1997;Pell et al 1998) and the attenuation of reperfusioninduced arrhythmias (Oxman et al 1997;Dow et al 2012), very little is known about the effect of RIPC on the incidence and severity of ischaemic tachyarrhythmias.…”

mentioning

confidence: 99%

Remote vs. local ischaemic preconditioning in the rat heart: infarct limitation, suppression of ischaemic arrhythmia and the role of reactive oxygen species

Galagudza

Sonin

Власов

et al. 2016

Int J Experimental Path

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SUMMARYThe unmet clinical need for myocardial salvage during ischaemia-reperfusion injury requires the development of new techniques for myocardial protection. In this study the protective effect of different local ischaemic preconditioning (LIPC) and remote ischaemic preconditioning (RIPC) protocols was compared in the rat model of myocardial ischaemia-reperfusion, using infarct size and ischaemic tachyarrhythmias as end-points. In addition, the hypothesis that there is involvement of reactive oxygen species (ROS) in the protective signalling by RIPC was tested, again in comparison with LIPC. The animals were subjected to 30-min coronary occlusion and 90-min reperfusion. RIPC protocol included either transient infrarenal aortic occlusion (for 5, 15 and 30 min followed by 15-min reperfusion) or 15-min mesenteric artery occlusion with 15-min reperfusion. Ventricular tachyarrhythmias during test ischaemia were quantified according to Lambeth Conventions. It was found that the infarct-limiting effect of RIPC critically depends on the duration of a single episode of remote ischaemia, which fails to protect the heart from infarction when it is too short or, instead, too prolonged. It was also shown that RIPC is ineffective in reducing the incidence and severity of ischaemia-induced ventricular tachyarrhythmias. According to our data, the infarct-limiting effect of LIPC could be partially eliminated by the administration of ROS scavenger N-2-mercaptopropionylglycine (90 mg/kg), whereas the same effect of RIPC seems to be independent of ROS signalling.

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“…Permite desde logo a redução da área de enfarte, do risco de arritmias de reperfusão 11,17 (nomeadamente extrassistolia, fibrilação e taquicardia ventricular 18 ) e preservação da função ventricular esquerda 19,20 .…”

Section: Mecanismos Fisiopatológicos Envolvidos No Pré-condicionamentunclassified

Pré-condicionamento isquémico remoto do miocárdio: dos mecanismos fisiopatológicos à aplicação na prática clínica

Costa

Fontes‐Carvalho

Leite‐Moreira

2013

Revista Portuguesa de Cardiologia

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Short periods of myocardial ischemia followed by reperfusion induce a cardioprotective mechanism when the myocardium is subsequently subjected to a prolonged period of ischemia, a phenomenon known as ischemic preconditioning. As well as its application in the myocardium, ischemic preconditioning can also be induced by brief interruptions of blood flow to other organs, particularly skeletal muscle. Transient ischemia induced noninvasively by inflating a cuff on a limb, followed by reperfusion, helps reduce the damage caused to the myocardium by interruption of the coronary circulation. Remote ischemic preconditioning involves activation of humoral and/or neural pathways that open mitochondrial ATP-sensitive potassium channels in the myocardium and close mitochondrial permeability transition pores, making cardiomyocytes less vulnerable to ischemia-induced cell death. This cardioprotective mechanism is now being translated into clinical practice, with positive results in several clinical trials in coronary artery bypass surgery, surgical repair of abdominal aortic aneurysms, valve replacement surgery and percutaneous coronary intervention. However, certain factors weaken the subcellular mechanisms of preconditioning - age, comorbidities, medication, anesthetic protocol - and appear to explain the heterogeneity of results in some studies. Detailed understanding of the pathways involved in cardioprotection induced by ischemic preconditioning is expected to lead to the development of new drugs to reduce the consequences of prolonged ischemia.

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The Effect of Acute Versus Delayed Remote Ischemic Preconditioning on Reperfusion Induced Ventricular Arrhythmias

Abstract: Acute RIPC of the lower limbs induced a powerful delay in/and reduction in IR induced ventricular arrhythmias, but without evoking the RISK pathway; a late protective phase of RIPC on arrhythmias did not occur.

Cited by 28 publications

References 42 publications

Myocardial triggers involved in activation of remote ischaemic preconditioning

Myocardial triggers involved in activation of remote ischaemic preconditioning

Remote vs. local ischaemic preconditioning in the rat heart: infarct limitation, suppression of ischaemic arrhythmia and the role of reactive oxygen species

Pré-condicionamento isquémico remoto do miocárdio: dos mecanismos fisiopatológicos à aplicação na prática clínica

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