Facilitation of ischaemia‐induced ventricular fibrillation by catecholamines is mediated by β1 and β2 agonism in the rat heart in vitro

Wilder, Catherine D. E.; Pavlaki, Nikoleta; Dursun, Tutku; Gyimah, Paul; Caldwell-Dunn, Ellice; Ranieri, Antonella; Lewis, Hannah R.; Curtis, Michael J.

doi:10.1111/bph.14176

Cited by 6 publications

(1 citation statement)

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“…Activation of sympathetic system predisposes to ischemia-induced VF [ 22 , 23 ] that can be based on several mechanisms mediated by catecholamine-related [ 24 ] as well as neuropeptide Y-related [ 25 ] signaling. The proarrhythmic effects of sympathetic activation include facilitation of ectopic activity by abnormal automaticity and afterdepolarizations [ 26 , 27 , 28 , 29 ], increase in DOR [ 30 ] and inhomogeneous conduction [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Prevents Early but Not Delayed Ventricular Fibrillation in the Experimental Porcine Model of Acute Ischemia

Tsvetkova

Bernikova

Mikhaleva

et al. 2020

IJMS

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Antiarrhythmic effects of melatonin have been demonstrated ex vivo and in rodent models, but its action in a clinically relevant large mammalian model remains largely unknown. Objectives of the present study were to evaluate electrophysiological and antiarrhythmic effects of melatonin in a porcine model of acute myocardial infarction. Myocardial ischemia was induced by 40-min coronary occlusion in 25 anesthetized pigs. After ischemia onset, 12 animals received melatonin (4 mg/kg). 48 intramyocardial electrograms were recorded from left ventricular wall and interventricular septum (IVS). In each lead, activation time (AT) and repolarization time (RT) were determined. During ischemia, ATs and dispersion of repolarization (DOR = RTmax − RTmin) increased reaching maximal values by 3–5 and 20–25 min, respectively. Ventricular fibrillation (VF) incidence demonstrated no relations to redox state markers and was associated with increased DOR and delayed ATs (specifically, in an IVS base, an area adjacent to the ischemic zone) (p = 0.031). Melatonin prevented AT increase in the IVS base, (p < 0.001) precluding development of early VF (1–5 min, p = 0.016). VF occurrence in the delayed phase (17–40 min) where DOR was maximal was not modified by melatonin. Thus, melatonin-related enhancement of activation prevented development of early VF in the myocardial infarction model.

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