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1. Antiarrhythmic mechanisms of Malbec wine and resveratrol in isolated rat heart

Author

Ponce Zumino Az, N F Renna, Parra M, Natalia Jorgelina Prado, Perdicaro Dj, E R Diez, Vazquez Prieto Ma, Carrion Am, and Roberto Miguel Miatello

Subjects
Wine, Farmacología y Farmacia, ARRHYTHMIAS, CIENCIAS MÉDICAS Y DE LA SALUD, business.industry, WINE, General Medicine, Rat heart, purl.org/becyt/ford/3.1 [https], Resveratrol, Pharmacology, Medicina Básica, chemistry.chemical_compound, chemistry, Medicine, purl.org/becyt/ford/3 [https], OXIDATIVE STRESS, business, RESVERATROL
Abstract

Oxidative stress during myocardial reperfusion contributes to ventricular arrhythmias onset. We aim to evaluate the antiarrhythmic effect of Malbec wine and resveratrol and compare them with the synthetic antioxidant tiron. Since alcohol use is controversial, we also assessed dealcoholized wine.Isolated hearts from male Sprague Dawley rats were perfused with Krebs-Henseleit solution added with: Malbec wine (5 ml/L), resveratrol (10 μM,) compared to controls with alcohol (0.5 ml/L); dealcoholized wine (5 ml/L), tiron (10 mM) were compared with controls without alcohol. Epicardial action potentials were analyzed during basal state, regional ischemia and reperfusion (10 minutes each period). The incidence of arrhythmias was determined. Te antioxidant effect was assessed in left ventricle homogenates and expressed as a percentage of inhibition of the ABTS?+ radical.Malbec wine and resveratrol reduced reperfusion arrhythmias in 56% and 50%, respectively, compared to 100% incidence in the control group with alcohol. Dealcoholized wine reduced arrhythmias to 50% compared to non-alcoholic control (90.5%), but tiron did not protect (69%). Te free radicals inhibitory effect increased with all the compounds (resveratrol 54.2%, tiron 43.2%, Malbec wine 42.9%, dealcoholized wine 40.2%) with respect to the control groups (with alcohol 23.5%, without alcohol 21.2%). Resveratrol shortened action potential duration and prevented ischemic depolarization. Malbec prevented ischemic-induced action potential shortening. We conclude that Malbec wine and resveratrol are antiarrhythmic beyond their antioxidant properties. Alcohol content or was not essential. Protection from ischemic action potential changes could be relevant to the antiarrhythmic effect of both resveratrol and wine. Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina Fil: Perdicaro DJ. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina Fil: Parra, M. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; Argentina Fil: Carrión AM. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; Argentina Fil: Miatello RM. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina Fil: Renna NF. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina Fil: Ponce Zumino AZ. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; Argentina Fil: Vazquez Prieto M. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina Fil: Diez ER. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina

Published
2018

2. Ischemic Postconditioning Reduces Reperfusion arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of KATP Channels or Connexin 43

Author

Natalia Jorgelina Prado, Emiliano Raúl Diez, Roberto Miguel Miatello, Amira Ponce Zumino, José Antonio Sánchez Sánchez, David Garcia-Dorado, Antonio Rodríguez-Sinovas, Institut Català de la Salut, [Diez ER, Prado NJ, Ponce Zumino AZ, Miatello RM] Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza 5500, Argentina. Institute of Medical and Experimental Biology of Cuyo, CONICET, Mendoza 5500, Argentina. [Sánchez JA, García-Dorado D, Rodríguez-Sinovas A] Grup Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain, and Vall d'Hebron Barcelona Hospital Campus

Subjects
0301 basic medicine, Adenosina, Connexin, 030204 cardiovascular system & hematology, Pharmacology, postconditioning, connexin 43, Glibenclamide, chemistry.chemical_compound, 0302 clinical medicine, PKC, Spectroscopy, education.field_of_study, Chemistry, Therapeutics::Ischemic Postconditioning [ANALYTICAL, DIAGNOSTIC AND THERAPEUTIC TECHNIQUES, AND EQUIPMENT], General Medicine, terapéutica::poscondicionamiento isquémico [TÉCNICAS Y EQUIPOS ANALÍTICOS, DIAGNÓSTICOS Y TERAPÉUTICOS], purl.org/becyt/ford/3.1 [https], Computer Science Applications, Medicina Básica, Connexin 32, purl.org/becyt/ford/3 [https], Arrhythmia, medicine.drug, CIENCIAS MÉDICAS Y DE LA SALUD, Arrítmia, Fisiología, arrhythmia, Catalysis, Inorganic Chemistry, Postconditioning, 03 medical and health sciences, medicine, KATP channels, Physical and Theoretical Chemistry, education, Molecular Biology, Protein kinase C, CONNEXIN 43, enfermedades cardiovasculares::enfermedades cardíacas::arritmias cardíacas [ENFERMEDADES], Organic Chemistry, REPERFUSION ARRHYTHMIAS, ISCHEMIC POSTCONDITIONING, ADENOSINE RECEPTORS, Adenosine, Adenosine receptor, adenosine receptors, Electrophysiology, 030104 developmental biology, Chelerythrine, Cardiovascular Diseases::Heart Diseases::Arrhythmias, Cardiac [DISEASES]
Abstract

Ischemic postconditioning (IPoC) reduces reperfusion arrhythmias but the antiarrhythmic mechanisms remain unknown. The aim of this study was to analyze IPoC electrophysiological effects and the role played by adenosine A1, A2A and A3 receptors, protein kinase C, ATP-dependent potassium (KATP) channels, and connexin 43. IPoC reduced reperfusion arrhythmias (mainly sustained ventricular fibrillation) in isolated rat hearts, an effect associated with a transient delay in epicardial electrical activation, and with action potential shortening. Electrical impedance measurements and Lucifer-Yellow diffusion assays agreed with such activation delay. However, this delay persisted during IPoC in isolated mouse hearts in which connexin 43 was replaced by connexin 32 and in mice with conditional deletion of connexin 43. Adenosine A1, A2A and A3 receptor blockade antagonized the antiarrhythmic effect of IPoC and the associated action potential shortening, whereas exogenous adenosine reduced reperfusion arrhythmias and shortened action potential duration. Protein kinase C inhibition by chelerythrine abolished the protective effect of IPoC but did not modify the effects on action potential duration. On the other hand, glibenclamide, a KATP inhibitor, antagonized the action potential shortening but did not interfere with the antiarrhythmic effect. The antiarrhythmic mechanisms of IPoC involve adenosine receptor activation and are associated with action potential shortening. However, this action potential shortening is not essential for protection, as it persisted during protein kinase C inhibition, a maneuver that abolished IPoC protection. Furthermore, glibenclamide induced the opposite effects. In addition, IPoC delays electrical activation and electrical impedance recovery during reperfusion, but these effects are independent of connexin 43. Fil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina Fil: Sánchez, Jose Antonio. Centro de Investigación Biomédica en Red sobre Enfermedades Cardiovasculares; España. Universidad Autonoma de Barcelona. Hospital Vall D' Hebron. Instituto de Investigación Vall D'hebron. Serv.de Cardiología,laboratorio de Cardiología Experimenta; España Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina Fil: Ponce Zumino, Amira Zulma. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina Fil: García-Dorado, David. Universidad Autonoma de Barcelona. Hospital Vall D' Hebron. Instituto de Investigación Vall D'hebron. Serv.de Cardiología,laboratorio de Cardiología Experimenta; España. Centro de Investigación Biomédica en Red sobre Enfermedades Cardiovasculares; España Fil: Miatello, Roberto Miguel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina Fil: Rodríguez-Sinovas, Antonio. Centro de Investigación Biomédica en Red sobre Enfermedades Cardiovasculares; España. Universidad Autonoma de Barcelona. Hospital Vall D' Hebron. Instituto de Investigación Vall D'hebron. Serv.de Cardiología,laboratorio de Cardiología Experimenta; España

Published
2019

3. Anti-inflammatory, antioxidant, antihypertensive, and antiarrhythmic effect of indole-3-carbinol, a phytochemical derived from cruciferous vegetables.

Author

Prado NJ, Ramirez D, Mazzei L, Parra M, Casarotto M, Calvo JP, Cuello Carrión D, Ponce Zumino AZ, Diez ER, Camargo A, and Manucha W

Abstract

Background: Cardiovascular inflammation and oxidative stress are determining factors in high blood pressure and arrhythmias. Indole-3-carbinol is a cruciferous-derived phytochemical with potential anti-inflammatory and antioxidant effects. However, its implications on the modulation of cardiovascular inflammatory-oxidative markers are unknown., Objectives: To establish the effects of indole-3-carbinol on the oxidative-inflammatory-proarrhythmic conditions associated with hypertension., Materials: Histological, biochemical, molecular, and functional aspects were evaluated in 1) Culture of mouse BV-2 glial cells subjected to oxidative-inflammatory damage by lipopolysaccharides (100 ng/mL) in the presence or absence of 40 μM indole-3-carbinol (n = 5); 2) Male spontaneously hypertensive rats (SHR) and Wistar Kyoto rats receiving indole-3-carbinol (2000 ppm/day, orally) during the first 8 weeks of life (n = 15); 3) Isolated rat hearts were submitted to 10 min regional ischemia and 10 min reperfusion., Results: 1) lipopolysaccharides induced oxidative stress and increased inflammatory markers; indole-3-carbinol reversed both conditions (interleukin 6, tumor necrosis factor α, the activity of nicotinamide adenine dinucleotide phosphate oxidase, nitric oxide, inducible nitric oxide synthase, heat shock protein 70, all p < 0.01 vs lipopolysaccharides). 2) SHR rats showed histological, structural, and functional changes with increasing systolic blood pressure (154 ± 8 mmHg vs. 122 ± 7 mmHg in Wistar Kyoto rats, p < 0.01); Inflammatory-oxidative markers also increased, and nitric oxide and heat shock protein 70 decreased. Conversely, indole-3-carbinol reduced oxidative-inflammatory markers and systolic blood pressure (133 ± 8 mmHg, p < 0.01 vs. SHR). 3) indole-3-carbinol reduced reperfusion arrhythmias from 8/10 in SHR to 0/10 (p = 0.0007 by Fisher's exact test)., Conclusions: Indole-3-carbinol reduces the inflammatory-oxidative-proarrhythmic process of hypertension. The nitric oxide and heat shock protein 70 are relevant mechanisms of indole-3-carbinol protective actions. Further studies with this pleiotropic phytochemical as a promising cardioprotective are guaranteed., Competing Interests: The authors declare no conflict of interest., (© 2022 The Author(s).)

Published
2022
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4. Reperfusion Arrhythmias Increase after Superior Cervical Ganglionectomy Due to Conduction Disorders and Changes in Repolarization.

Author

Prado NJ, Muñoz EM, Farias Altamirano LE, Aguiar F, Ponce Zumino AZ, Sánchez FJ, Miatello RM, Pueyo E, and Diez ER

Subjects
Animals, Arrhythmias, Cardiac etiology, Arrhythmias, Cardiac metabolism, Circadian Rhythm, Connexin 43 genetics, Connexin 43 metabolism, Male, Melatonin metabolism, Rats, Rats, Wistar, Receptors, Melatonin genetics, Receptors, Melatonin metabolism, Sarcoplasmic Reticulum Calcium-Transporting ATPases genetics, Sarcoplasmic Reticulum Calcium-Transporting ATPases metabolism, Arrhythmias, Cardiac pathology, Ganglionectomy adverse effects, Heart physiopathology, Myocardial Reperfusion Injury surgery
Abstract

Pharmacological concentrations of melatonin reduce reperfusion arrhythmias, but less is known about the antiarrhythmic protection of the physiological circadian rhythm of melatonin. Bilateral surgical removal of the superior cervical ganglia irreversibly suppresses melatonin rhythmicity. This study aimed to analyze the cardiac electrophysiological effects of the loss of melatonin circadian oscillation and the role played by myocardial melatonin membrane receptors, SERCA 2A , TNFα, nitrotyrosine, TGFβ, K ATP channels, and connexin 43. Three weeks after bilateral removal of the superior cervical ganglia or sham surgery, the hearts were isolated and submitted to ten minutes of regional ischemia followed by ten minutes of reperfusion. Arrhythmias, mainly ventricular tachycardia, increased during reperfusion in the ganglionectomy group. These hearts also suffered an epicardial electrical activation delay that increased during ischemia, action potential alternants, triggered activity, and dispersion of action potential duration. Hearts from ganglionectomized rats showed a reduction of the cardioprotective MT 2 receptors, the MT 1 receptors, and SERCA 2A . Markers of nitroxidative stress (nitrotyrosine), inflammation (TNFα), and fibrosis (TGFβ and vimentin) did not change between groups. Connexin 43 lateralization and the pore-forming subunit (Kir6.1) of K ATP channels increased in the experimental group. We conclude that the loss of the circadian rhythm of melatonin predisposes the heart to suffer cardiac arrhythmias, mainly ventricular tachycardia, due to conduction disorders and changes in repolarization.

Published
2020
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5. Ischemic Postconditioning Reduces Reperfusion Arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of K ATP Channels or Connexin 43.

Author

Diez ER, Sánchez JA, Prado NJ, Ponce Zumino AZ, García-Dorado D, Miatello RM, and Rodríguez-Sinovas A

Subjects
Adenosine Triphosphate metabolism, Animals, Arrhythmias, Cardiac etiology, Arrhythmias, Cardiac metabolism, Arrhythmias, Cardiac pathology, KATP Channels genetics, Mice, Mice, Transgenic, Protein Kinase C genetics, Rats, Rats, Sprague-Dawley, Receptors, Purinergic P1 genetics, Arrhythmias, Cardiac prevention & control, Connexin 43 physiology, Ischemic Postconditioning methods, KATP Channels metabolism, Myocardial Ischemia complications, Protein Kinase C metabolism, Receptors, Purinergic P1 metabolism
Abstract

Ischemic postconditioning (IPoC) reduces reperfusion arrhythmias but the antiarrhythmic mechanisms remain unknown. The aim of this study was to analyze IPoC electrophysiological effects and the role played by adenosine A 1 , A 2A and A 3 receptors, protein kinase C, ATP-dependent potassium (K ATP ) channels, and connexin 43. IPoC reduced reperfusion arrhythmias (mainly sustained ventricular fibrillation) in isolated rat hearts, an effect associated with a transient delay in epicardial electrical activation, and with action potential shortening. Electrical impedance measurements and Lucifer-Yellow diffusion assays agreed with such activation delay. However, this delay persisted during IPoC in isolated mouse hearts in which connexin 43 was replaced by connexin 32 and in mice with conditional deletion of connexin 43. Adenosine A 1 , A 2A and A 3 receptor blockade antagonized the antiarrhythmic effect of IPoC and the associated action potential shortening, whereas exogenous adenosine reduced reperfusion arrhythmias and shortened action potential duration. Protein kinase C inhibition by chelerythrine abolished the protective effect of IPoC but did not modify the effects on action potential duration. On the other hand, glibenclamide, a K ATP inhibitor, antagonized the action potential shortening but did not interfere with the antiarrhythmic effect. The antiarrhythmic mechanisms of IPoC involve adenosine receptor activation and are associated with action potential shortening. However, this action potential shortening is not essential for protection, as it persisted during protein kinase C inhibition, a maneuver that abolished IPoC protection. Furthermore, glibenclamide induced the opposite effects. In addition, IPoC delays electrical activation and electrical impedance recovery during reperfusion, but these effects are independent of connexin 43.

Published
2019
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