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臭氧暴露对心率变异性和应激激素的影响:一项随机交叉研究。

Impact of ozone exposure on heart rate variability and stress hormones: A randomized-crossover study.

机构信息

Department of Environmental Health, School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and NHC Key Lab of Health Technology Assessment, Fudan University, P.O. Box 249,130 Dong-An Road, Shanghai 200032, China.

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.

出版信息

J Hazard Mater. 2022 Jan 5;421:126750. doi: 10.1016/j.jhazmat.2021.126750. Epub 2021 Jul 26.

Abstract

The biological mechanisms underlying the associations between atmospheric ozone exposure and adverse cardiometabolic outcomes are yet to be identified. Imbalanced autonomic nervous system (ANS) as well as activations of the sympatho-adrenomedullary (SAM) and hypothalamic-pituitary-adrenal (HPA) axes are among possible early biological responses triggered by ozone, and may eventually lead to cardiometabolic abnormalities. To determine whether acute ozone exposure causes ANS imbalance and increases the secretion of neuroendocrine stress hormones, we conducted a randomized, double-blind, crossover trial, under controlled 2-hour exposure to either ozone (200 ppb) or clean air with intermittent exercise among 22 healthy young adults. Here we found that, compared to clean air exposure, acute ozone exposure significantly decreased the high-frequency band of heart rate variability, even after adjusting for heart rate and pre-exposure to ambient air pollutants and meteorological factors. Ozone exposure also significantly increased the serum levels of stress hormones, including corticotrophin-releasing factor, adrenocorticotropic hormone, adrenaline, and noradrenaline. Metabolomics analysis showed that acute ozone exposure led to alterations in stress hormones, systemic inflammation, oxidative stress, and energy metabolism. Our results suggest that acute ozone exposure may trigger ANS imbalance and activate the HPA and SAM axes, offering potential biological explanations for the adverse cardiometabolic effects following acute ozone exposure.

摘要

大气臭氧暴露与不良心血管代谢结局之间关联的生物学机制尚不清楚。失衡的自主神经系统(ANS)以及交感肾上腺髓质(SAM)和下丘脑-垂体-肾上腺(HPA)轴的激活,是臭氧可能引发的早期生物学反应之一,最终可能导致心血管代谢异常。为了确定急性臭氧暴露是否会导致 ANS 失衡并增加神经内分泌应激激素的分泌,我们在 22 名健康年轻成年人中进行了一项随机、双盲、交叉试验,在 2 小时的受控暴露下,他们分别暴露于臭氧(200 ppb)或清洁空气中,并伴有间歇性运动。在这里,我们发现与暴露于清洁空气相比,急性臭氧暴露显著降低了心率变异性的高频带,即使在调整了心率以及先前暴露于环境空气污染物和气象因素后也是如此。臭氧暴露还显著增加了应激激素的血清水平,包括促肾上腺皮质释放因子、促肾上腺皮质激素、肾上腺素和去甲肾上腺素。代谢组学分析表明,急性臭氧暴露导致应激激素、全身炎症、氧化应激和能量代谢的改变。我们的结果表明,急性臭氧暴露可能会引发 ANS 失衡并激活 HPA 和 SAM 轴,为急性臭氧暴露后不良心血管代谢影响提供潜在的生物学解释。

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