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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 7682569, 12 pages
Research Article

Proinflammatory Cytokines Are Soluble Mediators Linked with Ventricular Arrhythmias and Contractile Dysfunction in a Rat Model of Metabolic Syndrome

1Cátedra de Cardiología, Escuela de Medicina, Tecnológico de Monterrey, Monterrey, Mexico
2Centro de Investigación Biomédica, Hospital Zambrano Hellion, Tec Salud del Sistema Tecnológico de Monterrey, Monterrey, Mexico
3Centro de Investigación en Nutrición Clínica y Obesidad, Escuela de Medicina, Tecnológico de Monterrey, Monterrey, Mexico
4Laboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Ciudad de México, Mexico

Correspondence should be addressed to Gerardo García-Rivas

Received 1 April 2017; Accepted 27 August 2017; Published 19 October 2017

Academic Editor: Giuseppe Cirillo

Copyright © 2017 Evaristo Fernández-Sada et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Metabolic syndrome (MS) increases cardiovascular risk and is associated with cardiac dysfunction and arrhythmias, although the precise mechanisms are still under study. Chronic inflammation in MS has emerged as a possible cause of adverse cardiac events. Male Wistar rats fed with 30% sucrose in drinking water and standard chow for 25–27 weeks were compared to a control group. The MS group showed increased weight, visceral fat, blood pressure, and serum triglycerides. The most important increases in serum cytokines included IL-1β (7-fold), TNF-α (84%), IL-6 (41%), and leptin (2-fold), the latter also showing increased gene expression in heart tissue (35-fold). Heart function ex vivo in MS group showed a decreased mechanical performance response to isoproterenol challenge (ISO). Importantly, MS hearts under ISO showed nearly twofold the incidence of ventricular fibrillation. Healthy rat cardiomyocytes exposed to MS group serum displayed impaired contractile function and Ca2+ handling during ISO treatment, showing slightly decreased cell shortening and Ca2+ transient amplitude (23%), slower cytosolic calcium removal (17%), and more frequent spontaneous Ca2+ release events (7.5-fold). As spontaneous Ca2+ releases provide a substrate for ventricular arrhythmias, our study highlights the possible role of serum proinflammatory mediators in the development of arrhythmic events during MS.