1. Carbon monoxide exposure enhances arrhythmia after cardiac stress: involvement of oxidative stress
- Author
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Martine Delage, Cyril Reboul, Alain Lacampagne, Fares Gouzi, Christine Feillet-Coudray, Gilles Fouret, Aldja Abdellaoui, Jérôme Thireau, Lucas Andre, Julien Boissiere, Olivier Cazorla, Grégory Meyer, Jérémy Fauconnier, Philippe Obert, Maurice Hayot, Jean-Paul Cristol, Sylvain Richard, Physiopathologie cardiovasculaire, Université Montpellier 1 (UM1)-IFR3, Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM), EA4278 Laboratoire de Pharm-Ecologie Cardiovasculaire (LaPEC), Avignon Université (AU), Département de biochimie [Montpellier], Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie, Université de Montpellier (UM), Dynamique Musculaire et Métabolisme (DMEM), Institut National de la Recherche Agronomique (INRA)-Université de Montpellier (UM), Physiopathologie des adaptations cardiovasculaires à l'Exercice, This work was supported by a French National Research Agency grant (COMYOCARD). SR, JF, AL, and OC are scientists from the Centre National de la Recherche Scientifique. We thank Sandrine Gayrard for technical assistance., Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), and Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
- Subjects
Male ,Physiology ,030204 cardiovascular system & hematology ,medicine.disease_cause ,Ryanodine receptor 2 ,Lipid peroxidation ,chemistry.chemical_compound ,0302 clinical medicine ,11. Sustainability ,Homeostasis ,Myocytes, Cardiac ,rat ,ComputingMilieux_MISCELLANEOUS ,chemistry.chemical_classification ,0303 health sciences ,Carbon Monoxide ,medicine.diagnostic_test ,Cardiac stress test ,Malondialdehyde ,3. Good health ,cardiac and cardiovascular systems ,cardiology ,Cardiology ,cardiovascular system ,Cardiology and Cardiovascular Medicine ,signal transduction ,tachyarrhythmias ,maladies cardiovasculaires ,medicine.medical_specialty ,electrocardiography ,tachyarythmies ,Blotting, Western ,Diastole ,Sudden death ,03 medical and health sciences ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Physiology (medical) ,Internal medicine ,Air Pollution ,medicine ,Animals ,Rats, Wistar ,030304 developmental biology ,Reactive oxygen species ,calcium ,business.industry ,mortalité cardiaque ,Arrhythmias, Cardiac ,Rats ,Oxidative Stress ,chemistry ,13. Climate action ,arythmie cardiaque ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,business ,Reactive Oxygen Species ,Oxidative stress ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology - Abstract
International audience; Arrhythmias following cardiac stress are a key predictor of death in healthy population. Carbon monoxide (CO) is a ubiquitous pollutant promoting oxidative stress and associated with hospitalization for cardiovascular disease and cardiac mortality. We investigated the effect of chronic CO exposure on the occurrence of arrhythmic events after a cardiac stress test and the possible involvement of related oxidative stress. Wistar rats exposed chronically (4 weeks) to sustained urban CO pollution presented more arrhythmic events than controls during recovery after cardiac challenge with isoprenaline in vivo. Sudden death occurred in 22% of CO-exposed rats versus 0% for controls. Malondialdehyde (MDA), an end-product of lipid peroxidation, was increased in left ventricular tissue of CO-exposed rats. Cardiomyocytes isolated from CO-exposed rats showed higher reactive oxygen species (ROS) production (measured with MitoSox Red dye), higher diastolic Ca(2+) resulting from SR calcium leak and an higher occurrence of irregular Ca(2+) transients (measured with Indo-1) in comparison to control cells after a high pacing sequence. Acute treatment with a ROS scavenger (N-acetylcysteine, 20 mmol/L, 1 h) prevented this sequence of alterations and decreased the number of arrhythmic cells following high pacing. Chronic CO exposure promotes oxidative stress that alters Ca(2+) homeostasis (through RYR2 and SERCA defects) and thereby mediates the triggering of ventricular arrhythmia after cardiac stress that can lead to sudden death.
- Published
- 2011