Short-term secondhand smoke exposure decreases heart rate variability and increases arrhythmia susceptibility in mice
Short-term secondhand smoke exposure decreases heart rate variability and increases arrhythmia susceptibility in mice
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DOI：
10.1152/ajpheart.91535.2007
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发表时间：
2008-08-01
影响因子：
4.8
通讯作者：
Bonham, Ann C.
中科院分区：
文献类型：
--
作者：
Chen, Chao-Yin;Chow, Drin;Bonham, Ann C.
接触二手烟（SHS）是一种主要的室内空气污染物，与心血管发病率和死亡率（包括心律失常）的增加有关。然而，流行病学研究结果背后的机制尚不清楚。以心率变异性 (HRV) 降低为标志的心脏自主功能受损可能是根本原因。本研究利用了明确的短期 SHS 暴露（3 天，6 小时/天）对 HRV 的影响以及小鼠对心律失常的易感性。通过对有意识的小鼠使用心电图遥测记录，在每天暴露后的夜间以及暴露于 SHS 或过滤空气 3 天后的 24 小时测量时域中的 HRV 参数。暴露3天后测定对心律失常的易感性。暴露于低浓度的 SHS [总悬浮颗粒 (TSP)，2.4 +/- 3.2；和尼古丁，0.3 +/- 0.1 mg/m(3)]对 HRV 参数没有显着影响。相比之下，暴露于较高但仍与环境相关的SHS浓度（TSP，30 +/- 1；和尼古丁，5 +/- 1 mg/m(3)）显着降低HRV，从暴露第一天后开始，并在暴露最后一天后持续24小时。此外，暴露的小鼠表现出室性心律失常易感性和房室传导阻滞显着增加。数据表明，接触二手烟后，HRV 会降低，并且与心律失常易感性增加相关。这些数据提供了对暴露于二手烟的人类心血管发病率和死亡率增加的可能机制的见解。
Exposure to secondhand smoke (SHS), a major indoor air pollutant, is linked to increased cardiovascular morbidity and mortality, including cardiac arrhythmias. However, the mechanisms underlying the epidemiological findings are not well understood. Impaired cardiac autonomic function, indexed by reduced heart rate variability (HRV), may represent an underlying cause. The present study takes advantage of well-defined short-term SHS exposure (3 days, 6 h/day) on HRV and the susceptibility to arrhythmia in mice. With the use of electrocardiograph telemetry recordings in conscious mice, HRV parameters in the time domain were measured during the night after each day of exposure and 24 h after 3 days of exposure to either SHS or filtered air. The susceptibility to arrhythmia was determined after 3 days of exposure. Exposure to a low concentration of SHS [ total suspended particle (TSP), 2.4 +/- 3.2; and nicotine, 0.3 +/- 0.1 mg/m(3)] had no significant effect on HRV parameters. In contrast, the exposure to a higher but still environmentally relevant concentration of SHS (TSP, 30 +/- 1; and nicotine, 5 +/- 1 mg/m(3)) significantly reduced HRV starting after the first day of exposure and continuing 24 h after the last day of exposure. Moreover, the exposed mice showed a significant increase in ventricular arrhythmia susceptibility and atrioventricular block. The data suggest that SHS exposure decreased HRV beyond the exposure period and was associated with an increase in arrhythmia susceptibility. The data provide insights into possible mechanisms underlying documented increases in cardiovascular morbidity and mortality in humans exposed to SHS.