化石燃料的燃烧导致空气污染(AP),这与2018年全球约879万人死亡有关,主要是由于呼吸和心血管相关影响。其中,颗粒物空气污染(PM2.5)是心脏健康的主要危险因素,特别是在脆弱的阶段。我们先前的研究表明,过早暴露于1,2-萘醌(1,2-NQ),一种在柴油机废气颗粒(DEP)中发现的化学物质,在成年期加重哮喘。此外,1,2-NQ浓度的增加有助于PM2.5引发的气道炎症,采用与瞬时受体电位香草酸1(TRPV1)上调相关的神经源性途径。然而,尚未研究1,2-萘醌(1,2-NQ)早期暴露对心房颤动(AF)的潜在影响.这项研究旨在研究在生命早期吸入1,2-NQ如何影响自主神经肾上腺素能系统以及TRPV1在这些心脏病中的作用。将C57Bl/6新生雄性小鼠在生命的第6、8和10天暴露于1,2-NQ(100nM)或其载体。早期暴露于1,2-NQ会损害右心房的肾上腺素能反应,而不会显着影响胆碱能反应。心电图分析显示幼鼠的节律性改变,提示交感神经系统活动增加。此外,1,2-NQ影响β1-肾上腺素能受体激动剂介导的正慢性,美托洛尔可以预防,β1受体阻滞剂。卡沙西平,TRPV1阻断剂,但不是TRPC5阻断剂,逆转1,2-NQ诱导的心脏变化。总之,新生小鼠暴露于AP1,2-NQ导致发生心脏肾上腺素能功能障碍的风险升高,在年轻时可能导致房性心律失常。
The combustion of fossil fuels contributes to air pollution (AP), which was linked to about 8.79 million global deaths in 2018, mainly due to respiratory and cardiovascular-related effects. Among these, particulate air pollution (PM2.5) stands out as a major risk factor for heart health, especially during vulnerable phases. Our prior study showed that premature exposure to 1,2-naphthoquinone (1,2-NQ), a chemical found in diesel exhaust particles (DEP), exacerbated asthma in adulthood. Moreover, increased concentration of 1,2-NQ contributed to airway inflammation triggered by PM2.5, employing neurogenic pathways related to the up-regulation of transient receptor potential vanilloid 1 (TRPV1). However, the potential impact of early-life exposure to 1,2-naphthoquinone (1,2-NQ) on atrial fibrillation (AF) has not yet been investigated. This study aims to investigate how inhaling 1,2-NQ in early life affects the autonomic adrenergic system and the role played by TRPV1 in these heart disturbances. C57Bl/6 neonate male mice were exposed to 1,2-NQ (100 nM) or its vehicle at 6, 8, and 10 days of life. Early exposure to 1,2-NQ impairs adrenergic responses in the right atria without markedly affecting cholinergic responses. ECG analysis revealed altered rhythmicity in young mice, suggesting increased sympathetic nervous system activity. Furthermore, 1,2-NQ affected β1-adrenergic receptor agonist-mediated positive chronotropism, which was prevented by metoprolol, a β1 receptor blocker. Capsazepine, a TRPV1 blocker but not a TRPC5 blocker, reversed 1,2-NQ-induced cardiac changes. In conclusion, neonate mice exposure to AP 1,2-NQ results in an elevated risk of developing cardiac adrenergic dysfunction, potentially leading to atrial arrhythmia at a young age.