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Cardiac inotropic rebound effect after washout of acetylcholine is associated with electrophysiological heterogeneity in Langendorff-perfused rabbit heart

Cardiac electrophysiological heterogeneity related to the washout of acetylcholine (ACh) remains incompletely characterized. The aim of this study was to examine whether positive cardiac inotropic action is associated with electrophysiological heterogeneity between the atrium and the ventricle after...

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Detalles Bibliográficos
Autores principales: LUO, HAIJIAN, SI, JUNQIANG, ZHANG, FENGJIE, YANG, ZHENYU, WANG, RUXING
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919906/
https://www.ncbi.nlm.nih.gov/pubmed/24520282
http://dx.doi.org/10.3892/etm.2014.1486
Descripción
Sumario:Cardiac electrophysiological heterogeneity related to the washout of acetylcholine (ACh) remains incompletely characterized. The aim of this study was to examine whether positive cardiac inotropic action is associated with electrophysiological heterogeneity between the atrium and the ventricle after ACh perfusion and washout. Epicardial monophasic action potentials (MAPs) from the right ventricle and right atrium, as well as cardiac contractility, were recorded from isolated Langendorff-perfused rabbit hearts using MAP electrodes and a force transducer. The results indicated that rebound positive inotropic actions were induced by ACh washout with adrenaline preconditioning. This effect was accompanied by an increase in MAP amplitude (MAPA) in the right ventricle but not the right atrium. These findings indicate that cholinergic muscarinic stimulation may lead to positive cardiac inotropic action followed by changes in regional electrophysiological heterogeneity between the atrial and ventricular myocardium. Therefore, we hypothesize that electrophysiological heterogeneity is an underlying cause of arrhythmogenesis as well as hemodynamic disturbance elicited by sudden termination of vagus stimulation.