Center for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Center for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Redox Biol. 2020 Jul;34:101515. doi: 10.1016/j.redox.2020.101515. Epub 2020 Apr 18.
Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidative stress and inflammation in aortic, cardiac and/or cerebral tissues in single exposure models. In mice subjected to both stressors, most of these risk factors showed potentiated adverse changes. We also found that mice exposed to both noise and ATII had increased phagocytic NADPH oxidase (NOX-2)-mediated superoxide formation, immune cell infiltration (monocytes, neutrophils and T cells) in the aortic wall, astrocyte activation in the brain, enhanced cytokine signaling, and subsequent vascular and cerebral oxidative stress. Exaggerated renal stress response was also observed. In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. Mechanistically, noise potentiates neuroinflammation and cerebral oxidative stress, which may be a potential link between both risk factors. The results indicate that a combination of classical (arterial hypertension) and novel (noise exposure) risk factors may be deleterious for cardiovascular health.
动脉高血压是心血管疾病发展的最重要的风险因素。最近，飞机噪音已被证明与血压升高、内皮功能障碍和氧化应激有关。在这里，我们研究了飞机噪声与实验性动脉高血压联合作用时潜在的加剧心血管效应。C57BL/6J 小鼠连续 7 天接受 0.5mg/kg/d 的血管紧张素 II 输注，同时暴露于最大声压级为 85dB(A)、平均声压级为 72dB(A)的飞机噪声下 7 天，或同时暴露于两种应激源下。在单一暴露模型中，噪声和血管紧张素 II 增加了血压、内皮功能障碍、氧化应激和主动脉、心脏和/或大脑组织中的炎症。在同时受到两种应激源作用的小鼠中，大多数这些危险因素表现出增强的不良变化。我们还发现，同时暴露于噪声和 ATII 的小鼠在主动脉壁中具有增加的吞噬 NADPH 氧化酶 (NOX-2) 介导的超氧化物形成、免疫细胞浸润（单核细胞、中性粒细胞和 T 细胞）、大脑中的星形胶质细胞激活、增强的细胞因子信号传导以及随后的血管和大脑氧化应激。还观察到肾脏应激反应的加剧。总之，我们的结果表明，环境噪声暴露和动脉高血压之间存在增强的不良心血管效应，这主要是由血管炎症和氧化应激触发的。从机制上讲，噪声增强了神经炎症和大脑氧化应激，这可能是两种危险因素之间的潜在联系。研究结果表明，经典（动脉高血压）和新型（噪声暴露）风险因素的组合可能对心血管健康有害。
