Carbon monoxide pollution impairs myocardial perfusion reserve: implication of coronary endothelial dysfunction
| Autor: | Stéphane Tanguy, C. Rugale, Sandrine Gayrard, Cyril Reboul, Grégory Meyer, Phillippe Obert, Bernard Jover, Julien Boissiere |
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| Přispěvatelé: | Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Physiopathologie des adaptations cardiovasculaires à l'Exercice, Avignon Université (AU), Physiologie cardio-Respiratoire Expérimentale Théorique et Appliquée (TIMC-IMAG-PRETA), Techniques de l'Ingénierie Médicale et de la Complexité - Informatique, Mathématiques et Applications, Grenoble - UMR 5525 (TIMC-IMAG), VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP )-Centre National de la Recherche Scientifique (CNRS)-Université Joseph Fourier - Grenoble 1 (UJF)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP )-Centre National de la Recherche Scientifique (CNRS)-Université Joseph Fourier - Grenoble 1 (UJF), Aide à la Décision pour une Médecine Personnalisé - Laboratoire de Biostatistique, Epidémiologie et Recherche Clinique - EA 2415 (AIDMP), Université Montpellier 1 (UM1)-Université de Montpellier (UM) |
| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Male
MESH: Air Pollutants Environmental pollution Vasodilation Fractional flow reserve 030204 cardiovascular system & hematology Toxicology 0302 clinical medicine Enos 11. Sustainability Medicine MESH: Coronary Vessels MESH: Animals Endothelial dysfunction Inhalation exposure Air Pollutants Carbon Monoxide Inhalation Exposure 0303 health sciences biology Heart Coronary Vessels Fractional Flow Reserve Myocardial medicine.anatomical_structure Cardiology MESH: Inhalation Exposure MESH: Endothelium Vascular Cardiology and Cardiovascular Medicine Perfusion MESH: Carbon Monoxide MESH: Nitric Oxide Synthase Type III Nitroprusside medicine.medical_specialty MESH: Hemodynamics MESH: Myocardium Nitric Oxide Synthase Type III Endothelium MESH: Rats MESH: Vasodilation 03 medical and health sciences [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system Internal medicine Animals Rats Wistar Molecular Biology 030304 developmental biology MESH: Capillaries business.industry MESH: Acetylcholine Myocardium Hemodynamics MESH: Rats Wistar biology.organism_classification medicine.disease Acetylcholine MESH: Male MESH: Nitroprusside Capillaries Rats MESH: Fractional Flow Reserve Myocardial MESH: Heart 13. Climate action Endothelium Vascular business |
| Zdroj: | Cardiovascular Toxicology Cardiovascular Toxicology, Humana Press, 2011, 11 (4), pp.334-40. ⟨10.1007/s12012-011-9125-z⟩ |
| ISSN: | 1530-7905 |
| Popis: | International audience; Chronic exposure to simulated urban CO pollution is reported to be associated with cardiac dysfunction. Despite the potential implication of myocardial perfusion alteration in the pathophysiology of CO pollution, the underlying mechanisms remain today still unknown. Therefore, the aim of this work was to evaluate the effects of prolonged exposure to simulated urban CO pollution on the regulation of myocardial perfusion. Cardiac hemodynamics and myocardial perfusion were assessed under basal conditions and during the infusion of a β-Adrenergic agonist. The effects of CO exposure on capillary density, coronary endothelium-dependent vasodilatation, eNOS expression and eNOS uncoupling were also evaluated. Our main results were that prolonged CO exposure was associated with a blunted myocardial perfusion response to a physiological stress responsible for an altered contractile reserve. The impairment of myocardial perfusion reserve was not accounted for a reduced capillary density but rather by an alteration in coronary endothelium-dependent vasorelaxation (-45% of maximal relaxation to ACh). In addition, though chronic CO exposure did not change eNOS expression, it significantly increased eNOS uncoupling. Therefore, the present work underlines the fact that chronic CO exposure, at levels found in urban air pollution, is associated with reduced myocardial perfusion reserve. This phenomenon is explained at the coronary-vessel level by deleterious effects of CO exposure on the endothelium NO-dependent vasorelaxation via eNOS uncoupling. |
| Databáze: | OpenAIRE |
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