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首页> 外文期刊>Toxicology and Applied Pharmacology >TRPA1 mediates the cardiac effects of acrolein through parasympathetic dominance but also sympathetic modulation in mice
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TRPA1 mediates the cardiac effects of acrolein through parasympathetic dominance but also sympathetic modulation in mice

机译：TRPA1通过副交感神经统治地介导丙烯醛的心脏作用，但在小鼠中也有交感神经调节

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Numerous studies have demonstrated that short-term air pollution exposure causes cardiac autonomic imbalance as measured by heart rate variability (HRV). We previously showed that a single exposure to acrolein, a ubiquitous gaseous component of air pollution, not only causes autonomic imbalance, but also increases arrhythmia through transient receptor potential A1 (TRPA1) cation channels. Thus, the goal of this study was to characterize acrolein-induced autonomic changes in both normal and TRPA1-knockout mice (KO). Conscious, unrestrained C57BL/6 (WT) and KO mice were exposed to 3 ppm acrolein for 3 h. Separate groups were treated with either atenolol (sympathetic blocker), atropine (parasympathetic blocker) or hexamethonium (autonomic neuro-transmission blocker), immediately before exposure. Electrocardiogram (ECG) and heart rate (HR) were recorded continuously before, during and after exposure. Exposure to acrolein produced significant increases in standard deviation of normal-to-normal R-R intervals (SDNN), Root Mean Square of the Successive Differences (RMSSD) and Low-Frequency (LF), as well as an increase in arrhythmia in WT mice. Treatment with atenolol reduced this response while atropine enhanced it, and both drugs blocked the acrolein-induced increase in arrhythmia; hexamethonium had no effect. On the other hand, neither acrolein nor any drug had an effect in the KO mice. Thus, acrolein-induced HRV responses appear to be mediated by a combined parasympathetic and sympathetic modulation. KO mice did not demonstrate any increases in HRV with exposure to acrolein. These data demonstrate that the cardiac effects of irritant air pollutants likely involve disruption of homeostatic balance and altered regulation even in healthy animals.
机译：大量研究表明，短期空气污染暴露会导致心率变异性（HRV）测量的心脏自主神经失衡。我们之前的研究表明，单次接触丙烯醛（空气污染中普遍存在的气体成分）不仅会导致自主神经失衡，还会通过瞬时受体电位A1（TRPA1）阳离子通道增加心律失常。因此，本研究的目的是描述正常和TRPA1基因敲除小鼠（KO）中丙烯醛诱导的自主神经变化。清醒、不受限制的C57BL/6（WT）和KO小鼠暴露于3ppm丙烯醛中3h。在暴露前，分别用阿替洛尔（交感神经阻滞剂）、阿托品（副交感神经阻滞剂）或六甲铵（自主神经传导阻滞剂）治疗。在暴露前、暴露期间和暴露后连续记录心电图（ECG）和心率（HR）。暴露于丙烯醛后，WT小鼠的正常至正常R-R间期（SDNN）、连续差均方根（RMSSD）和低频率（LF）的标准差显著增加，心律失常也显著增加。阿替洛尔治疗减少了这种反应，而阿托品增强了这种反应，两种药物都阻止了丙烯醛引起的心律失常增加；六甲铵没有效果。另一方面，丙烯醛或任何药物对KO小鼠均无影响。因此，丙烯醛诱导的HRV反应似乎是由副交感神经和交感神经共同调节的。KO小鼠暴露于丙烯醛后，HRV没有任何增加。这些数据表明，刺激性空气污染物对心脏的影响可能包括体内平衡的破坏和调节的改变，即使是在健康的动物身上。

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