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Effets cardiovasculaires de polluants atmosphériques d'origine automobile : Etude par inhalation chez le rat de l'effet du NO2 seul et en mélange dans des gaz d'échappement de moteur Diesel.

Abstract : Air pollution from car traffic is a major health issue and is recognized as an importantrisk factor for cardiovascular disease. The contribution of the particulate phase of Diesel engine emissions to these health effects has been well established. However, studies on the gas phase are few in number, while the evolution of the depollution systems allowing a reduction of the Diesel particles, led to an increase in pollutants of the gas phases such as nitrogen dioxide (NO2) a major and toxic pollutant. consequently, the general objective of this work was to evaluate the attributable part of the gaseous phase, and more specifically NO2, in the cardiovascular effects induced by Diesel emissions representative of the current fleet. In a first step, a comparative study was conducted in the Wistar rat exposed by inhalation to NO2 alone or to Diesel emissions, producing NO2, and taken upstream and downstream of a particulate filter (PF). In order to understand the mechanisms of action involved, mitochondrial function and oxidative stress were evaluated, in parallel with cardiacfunction measurements after a single exposure (a single exposure of 3 h) and after repeated exposure (3 h / day, 5 days / week for 3 weeks). Second, a more specific study on the effects of NO2 on vascular function and its possible consequences in a hypertension model was carried out using two experimental models: a physiological model (Wistar rat) and a model of hypertension (SHR). Evaluation of the vascular function was performed by an ex vivo approach from isolated coronary arteries following single and repeated exposures in the Wistar rat and only after a single exposure in the SHR. For the latter, repeated exposures were also performed to explore mitochondrial function. Our results show that single exposure to emissions upstream and downstream of PF induces a slight alteration of cardiac function, which is more important at 5 ppm NO2 but reversible. After three weeks of repeated exposure, cardiac dysfunction persists as ventricular diameters remain high the day after the last exposure, both after exposures to upstream and downstream Diesel emissions and to NO2. Cardiac dysfunction is accompanied by an alteration in the vasorelaxation of the arteries exposed to NO2. In parallel with these alterations, weobserved mitochondrial dysfunction, particularly during NO2 exposures independently of myocardial or systemic oxidative stress. Exposure to NO2 aggravates pre-existingmitochondrial dysfunction during hypertension, suggesting worsening of cardiovascular function. All these results demonstrate the effect of the gaseous phase, in particular NO2, on the mitochondrial function in the two experimental models, indicating the importance of taking into account the action of the gas phase in the depollution systems to come up.
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https://tel.archives-ouvertes.fr/tel-01780687
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Submitted on : Friday, April 27, 2018 - 5:29:12 PM
Last modification on : Wednesday, October 14, 2020 - 3:34:34 AM

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  • HAL Id : tel-01780687, version 1

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Ahmed Karoui. Effets cardiovasculaires de polluants atmosphériques d'origine automobile : Etude par inhalation chez le rat de l'effet du NO2 seul et en mélange dans des gaz d'échappement de moteur Diesel.. Toxicologie. Normandie Université, 2017. Français. ⟨NNT : 2017NORMR135⟩. ⟨tel-01780687⟩

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