Melatonin prevents reperfusion arrhythmias by receptor-dependent and independent electrophysiological effects

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68407700%3A21460%2F18%3A00325382" target="_blank" >RIV/68407700:21460/18:00325382 - isvavai.cz</a>

Výsledek na webu

<a href="https://academic.oup.com/eurheartj/article/39/suppl_1/ehy565.P2836/5084239" target="_blank" >https://academic.oup.com/eurheartj/article/39/suppl_1/ehy565.P2836/5084239</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1093/eurheartj/ehy565.P2836" target="_blank" >10.1093/eurheartj/ehy565.P2836</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Melatonin prevents reperfusion arrhythmias by receptor-dependent and independent electrophysiological effects

Popis výsledku v původním jazyce

Introduction: Ventricular arrhythmias are complications during reperfusion of acute coronary syndromes. Melatonin reduces the incidence and duration of ventricular arrhythmias, but its protective mechanism remains elusive. This study aimed to investigate whether melatonin receptors contribute to an activation or/and repolarization as the antiarrhythmic action during reperfusion. Methods: Open-chest anesthetized female rats underwent regional ischemia for eight minutes to induce reperfusion arrhythmias. Before reperfusion, four groups of animals intravenously received: melatonin (4 mg/kg), a melatonin receptor blocker (luzindole 0.4 mg/kg), melatonin + luzindole, or placebo. Unipolar electrograms were recorded from ischemic and nonischemic areas using an array of 64-electrodes to obtain the activation time, repolarization time and dispersion of repolarization. Results: Melatonin reduced reperfusion arrhythmias (1 of 9 vs. controls 11 of 16, P=0.0112). Luzindole made the protection disappear (luzindole 4 of 6, luzindole + melatonin 6 of 8; both n.s.). Luzindole increased activation time in the reperfused area (luzindole 14.6 ms, melatonin + luzindole 15.1 vs. control 11.7 ms and melatonin 11.0 ms, P<0.05). Melatonin prevented the shortening in the repolarization time in the reperfused area, leading to homogenous repolarization. Melatonin and melatonin + luzindole decreased the dispersion of repolarization (melatonin 3.1 ms, melatonin + luzindole 4.2 ms vs. control 13.1 ms and luzindole 9.6 ms, P<0.05). Conclusion: Melatonin reduces dispersion of repolarization through a receptor-independent mechanism, but its antiarrhythmic effect also requires preservation of activation through a receptor-dependent mechanism. Our results in hearts in situ support its potential translation towards the clinic.

Název v anglickém jazyce

Melatonin prevents reperfusion arrhythmias by receptor-dependent and independent electrophysiological effects

Popis výsledku anglicky

Introduction: Ventricular arrhythmias are complications during reperfusion of acute coronary syndromes. Melatonin reduces the incidence and duration of ventricular arrhythmias, but its protective mechanism remains elusive. This study aimed to investigate whether melatonin receptors contribute to an activation or/and repolarization as the antiarrhythmic action during reperfusion. Methods: Open-chest anesthetized female rats underwent regional ischemia for eight minutes to induce reperfusion arrhythmias. Before reperfusion, four groups of animals intravenously received: melatonin (4 mg/kg), a melatonin receptor blocker (luzindole 0.4 mg/kg), melatonin + luzindole, or placebo. Unipolar electrograms were recorded from ischemic and nonischemic areas using an array of 64-electrodes to obtain the activation time, repolarization time and dispersion of repolarization. Results: Melatonin reduced reperfusion arrhythmias (1 of 9 vs. controls 11 of 16, P=0.0112). Luzindole made the protection disappear (luzindole 4 of 6, luzindole + melatonin 6 of 8; both n.s.). Luzindole increased activation time in the reperfused area (luzindole 14.6 ms, melatonin + luzindole 15.1 vs. control 11.7 ms and melatonin 11.0 ms, P<0.05). Melatonin prevented the shortening in the repolarization time in the reperfused area, leading to homogenous repolarization. Melatonin and melatonin + luzindole decreased the dispersion of repolarization (melatonin 3.1 ms, melatonin + luzindole 4.2 ms vs. control 13.1 ms and luzindole 9.6 ms, P<0.05). Conclusion: Melatonin reduces dispersion of repolarization through a receptor-independent mechanism, but its antiarrhythmic effect also requires preservation of activation through a receptor-dependent mechanism. Our results in hearts in situ support its potential translation towards the clinic.

Druh

O - Ostatní výsledky

CEP obor

—

OECD FORD obor

30109 - Pathology

Projekt

—

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2018

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů