British journal of pharmacology · 2026
Pharmacological treatment with a GABA(A) receptor modulator and a selective serotonin reuptake inhibitor as a mitigation strategy against aircraft noise-induced cardiovascular and neuronal damage.
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Kuntić Ivana, Kuntić Marin, Zheng Jiayin, Nardi Leonardo, Oelze Matthias, Valar Arijan, Mihaliková Dominika, Strohm Lea, Buchholz Hans-Georg, Bausbacher Nicole, Lange Simon, Ubbens Henning, Tang Qi, Zhang Liyu, Horta Guilherme, Stamm Paul, Hahad Omar, Methner Axel, Steven Sebastian, Li Huige, Schreckenberger Mathias, Krueger-Burg Dilja, Gericke Adrian, Schmeisser Michael J, Münzel Thomas, Daiber Andreas
Аннотация
BACKGROUND AND PURPOSE: Noise pollution, particularly by aircraft, is a significant risk factor for cardiovascular disease. Aircraft noise activates stress response pathways in the brain, via the amygdala, the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis.
EXPERIMENTAL APPROACH: Male C57BL/6J mice were treated with citalopram (a selective serotonin (5-HT)-reuptake inhibitor) or diazepam (a benzodiazepine) 1 day before aircraft noise exposure for 4 days. Aortic vascular function was measured by isometric tension method, microvascular function by video microscopy in pressurized cerebral arterioles, blood pressure by tail cuff, reactive oxygen species formation by dihydrothidium staining of vascular tissue and markers of inflammation and oxidative stress by western blotting.
KEY RESULTS: In support of the stress response concept, we report here that noise exposure of mice implicates an increase in activity primarily in the left amygdala, envisaged by [18F]fluorodeoxyglucose positron emission tomography (PET) scan. Both neuro-active drugs, diazepam and citalopram, ameliorated the adverse cardiovascular and neurobiological effects of noise exposure, partially preventing blood pressure increases and endothelial dysfunction in both large (aorta) and small vessels (cerebral arterioles). Diazepam showed slightly greater efficacy. Noise exposure also increased markers of oxidative stress and inflammation in the heart and brain (cortex and hippocampus), and both drugs mostly prevented these pathophysiological changes.
CONCLUSION AND IMPLICATIONS: The study provides indirect evidence that modulating the stress response pathway may represent a pharmacological approach to mitigate the negative effects of noise exposure. This may have implications for patients with neuropsychiatric disease suffering from aircraft noise exposure.
EXPERIMENTAL APPROACH: Male C57BL/6J mice were treated with citalopram (a selective serotonin (5-HT)-reuptake inhibitor) or diazepam (a benzodiazepine) 1 day before aircraft noise exposure for 4 days. Aortic vascular function was measured by isometric tension method, microvascular function by video microscopy in pressurized cerebral arterioles, blood pressure by tail cuff, reactive oxygen species formation by dihydrothidium staining of vascular tissue and markers of inflammation and oxidative stress by western blotting.
KEY RESULTS: In support of the stress response concept, we report here that noise exposure of mice implicates an increase in activity primarily in the left amygdala, envisaged by [18F]fluorodeoxyglucose positron emission tomography (PET) scan. Both neuro-active drugs, diazepam and citalopram, ameliorated the adverse cardiovascular and neurobiological effects of noise exposure, partially preventing blood pressure increases and endothelial dysfunction in both large (aorta) and small vessels (cerebral arterioles). Diazepam showed slightly greater efficacy. Noise exposure also increased markers of oxidative stress and inflammation in the heart and brain (cortex and hippocampus), and both drugs mostly prevented these pathophysiological changes.
CONCLUSION AND IMPLICATIONS: The study provides indirect evidence that modulating the stress response pathway may represent a pharmacological approach to mitigate the negative effects of noise exposure. This may have implications for patients with neuropsychiatric disease suffering from aircraft noise exposure.