Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage
Noise pollution is a known health risk factor and evidence for cardiovascular diseases associated with traffic noise is growing. At least 20% of the European Union’s population lives in noise-polluted areas with exposure levels exceeding the recommended limits of the World Health Organization, which...
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2025-01-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/14/1/59 |
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| author | Marin Kuntić Ivana Kuntić Jiayin Zheng Leonardo Nardi Matthias Oelze Arijan Valar Dominika Mihaliková Lea Strohm Henning Ubbens Qi Tang Liyu Zhang Guilherme Horta Paul Stamm Omar Hahad Dilja Krueger-Burg Huige Li Sebastian Steven Adrian Gericke Michael J. Schmeisser Thomas Münzel Andreas Daiber |
| author_facet | Marin Kuntić Ivana Kuntić Jiayin Zheng Leonardo Nardi Matthias Oelze Arijan Valar Dominika Mihaliková Lea Strohm Henning Ubbens Qi Tang Liyu Zhang Guilherme Horta Paul Stamm Omar Hahad Dilja Krueger-Burg Huige Li Sebastian Steven Adrian Gericke Michael J. Schmeisser Thomas Münzel Andreas Daiber |
| author_sort | Marin Kuntić |
| collection | DOAJ |
| description | Noise pollution is a known health risk factor and evidence for cardiovascular diseases associated with traffic noise is growing. At least 20% of the European Union’s population lives in noise-polluted areas with exposure levels exceeding the recommended limits of the World Health Organization, which is considered unhealthy by the European Environment Agency. This results in the annual loss of 1.6 million healthy life years. Here, we investigated the protective effects of cardiovascular drug interventions against aircraft noise-mediated cardiovascular complications such as elevated oxidative stress or endothelial dysfunction. Using our established mouse exposure model, we applied mean sound pressure levels of 72 dB(A) for 4 d. C57BL/6 mice were treated with the beta-blocker propranolol (15 mg/kg/d s.c. for 5 d) or the alpha-blocker phenoxybenzamine (1.5 mg/kg/d s.c. for 5 d) and noise-exposed for the last 4 d of the drug administration. Short-term noise exposure caused hypertension (measured by tail-cuff blood pressure monitoring) and impaired endothelial function (measured by isometric tension recording in the aorta and video microscopy in cerebral arterioles in response to acetylcholine). Noise also increased markers of oxidative stress and inflammation. Treatment of mice with propranolol and phenoxybenzamine prevented endothelial and microvascular dysfunction, which was supported by a decrease in markers of inflammation and oxidative stress in heart tissue and the brain. Amelioration of noise-induced hypertension (systolic blood pressure) was not observed, whereas pulse pressure was lowered by trend. This study provides a novel perspective mitigating the adverse effects of noise pollution, especially in vulnerable groups with medication, a rationale for further pharmacological human studies. |
| format | Article |
| id | doaj-art-4e91bce2a3064711a5a6991950d8df80 |
| institution | Kabale University |
| issn | 2076-3921 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj-art-4e91bce2a3064711a5a6991950d8df802025-01-24T13:19:21ZengMDPI AGAntioxidants2076-39212025-01-011415910.3390/antiox14010059Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and DamageMarin Kuntić0Ivana Kuntić1Jiayin Zheng2Leonardo Nardi3Matthias Oelze4Arijan Valar5Dominika Mihaliková6Lea Strohm7Henning Ubbens8Qi Tang9Liyu Zhang10Guilherme Horta11Paul Stamm12Omar Hahad13Dilja Krueger-Burg14Huige Li15Sebastian Steven16Adrian Gericke17Michael J. Schmeisser18Thomas Münzel19Andreas Daiber20Laboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyInstitute of Anatomy, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyDepartment of Ophthalmology, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyDepartment of Ophthalmology, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyInstitute of Anatomy, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyInstitute of Anatomy, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyGerman Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyDepartment of Ophthalmology, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyInstitute of Anatomy, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyLaboratory of Molecular Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, GermanyNoise pollution is a known health risk factor and evidence for cardiovascular diseases associated with traffic noise is growing. At least 20% of the European Union’s population lives in noise-polluted areas with exposure levels exceeding the recommended limits of the World Health Organization, which is considered unhealthy by the European Environment Agency. This results in the annual loss of 1.6 million healthy life years. Here, we investigated the protective effects of cardiovascular drug interventions against aircraft noise-mediated cardiovascular complications such as elevated oxidative stress or endothelial dysfunction. Using our established mouse exposure model, we applied mean sound pressure levels of 72 dB(A) for 4 d. C57BL/6 mice were treated with the beta-blocker propranolol (15 mg/kg/d s.c. for 5 d) or the alpha-blocker phenoxybenzamine (1.5 mg/kg/d s.c. for 5 d) and noise-exposed for the last 4 d of the drug administration. Short-term noise exposure caused hypertension (measured by tail-cuff blood pressure monitoring) and impaired endothelial function (measured by isometric tension recording in the aorta and video microscopy in cerebral arterioles in response to acetylcholine). Noise also increased markers of oxidative stress and inflammation. Treatment of mice with propranolol and phenoxybenzamine prevented endothelial and microvascular dysfunction, which was supported by a decrease in markers of inflammation and oxidative stress in heart tissue and the brain. Amelioration of noise-induced hypertension (systolic blood pressure) was not observed, whereas pulse pressure was lowered by trend. This study provides a novel perspective mitigating the adverse effects of noise pollution, especially in vulnerable groups with medication, a rationale for further pharmacological human studies.https://www.mdpi.com/2076-3921/14/1/59aircraft noise exposurehigh blood pressureendothelial dysfunctionoxidative stressinflammationpreventive therapy |
| spellingShingle | Marin Kuntić Ivana Kuntić Jiayin Zheng Leonardo Nardi Matthias Oelze Arijan Valar Dominika Mihaliková Lea Strohm Henning Ubbens Qi Tang Liyu Zhang Guilherme Horta Paul Stamm Omar Hahad Dilja Krueger-Burg Huige Li Sebastian Steven Adrian Gericke Michael J. Schmeisser Thomas Münzel Andreas Daiber Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage Antioxidants aircraft noise exposure high blood pressure endothelial dysfunction oxidative stress inflammation preventive therapy |
| title | Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage |
| title_full | Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage |
| title_fullStr | Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage |
| title_full_unstemmed | Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage |
| title_short | Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage |
| title_sort | interventions by cardiovascular drugs against aircraft noise induced cardiovascular oxidative stress and damage |
| topic | aircraft noise exposure high blood pressure endothelial dysfunction oxidative stress inflammation preventive therapy |
| url | https://www.mdpi.com/2076-3921/14/1/59 |
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