Whole and Particle-Free Diesel Exhausts Differentially Affect Cardiac Electrophysiology, Blood Pressure, and Autonomic Balance in Heart Failure-Prone Rats
Whole and Particle-Free Diesel Exhausts Differentially Affect Cardiac Electrophysiology, Blood Pressure, and Autonomic Balance in Heart Failure-Prone Rats
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DOI：
10.1093/toxsci/kfs162
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发表时间：
2012-08-01
影响因子：
3.8
通讯作者：
Farraj, Aimen K.
中科院分区：
文献类型：
--
作者：
Carll, Alex P.;Hazari, Mehdi S.;Farraj, Aimen K.
流行病学研究将短期暴露于车辆交通和颗粒物（PM）空气污染与不良心血管（CV）事件密切相关，特别是在既存CV疾病的患者中。柴油机排气是城市环境PM和气态污染物的主要贡献者。为了确定气体和颗粒成分在柴油机尾气（DE）心脏毒性中的作用，我们检测了4小时吸入全DE（wDE）（目标PM浓度：500 μ g/m3）或无颗粒过滤DE（fDE）对高血压心力衰竭易感大鼠CV生理学和一系列心肺损伤标志物的影响。监测动脉血压（BP）、心电图和心率变异性（HRV）（自主神经平衡的指标）。暴露期间fDE和wDE均降低血压和延长PR间期，fDE的作用更大，其还增加了HRV三角指数和降低了T波振幅。暴露后fDE立即增加QTc间期，此后不久增加房室（AV）阻滞Mobitz II心律失常，1天后增加血清高密度脂蛋白。wDE增加BP和降低HRV的根均方的连续差异立即后exexexplanation。fDE和wDE在暴露后4小时内降低心率。因此，DE气体减慢AV传导和心室复极，降低BP，增加HRV，随后引起心律失常，共同表明副交感神经激活;相反，暴露于含颗粒DE后的短暂BP和HRV变化表明短暂的交感神经兴奋。我们的研究结果表明，整个和颗粒自由DE差异改变CV和自主生理，并可能通过不同的途径增加风险。
Epidemiological studies strongly link short-term exposures to vehicular traffic and particulate matter (PM) air pollution with adverse cardiovascular (CV) events, especially in those with preexisting CV disease. Diesel engine exhaust is a key contributor to urban ambient PM and gaseous pollutants. To determine the role of gaseous and particulate components in diesel exhaust (DE) cardiotoxicity, we examined the effects of a 4-h inhalation of whole DE (wDE) (target PM concentration: 500 mu g/m(3)) or particle-free filtered DE (fDE) on CV physiology and a range of markers of cardiopulmonary injury in hypertensive heart failure prone rats. Arterial blood pressure (BP), electrocardiography, and heart rate variability (HRV), an index of autonomic balance, were monitored. Both fDE and wDE decreased BP and prolonged PR interval during exposure, with more effects from fDE, which additionally increased HRV triangular index and decreased T-wave amplitude. fDE increased QTc interval immediately after exposure, increased atrioventricular (AV) block Mobitz II arrhythmias shortly thereafter, and increased serum high-density lipoprotein 1 day later. wDE increased BP and decreased HRV root mean square of successive differences immediately postexposure. fDE and wDE decreased heart rate during the 4th hour of postexposure. Thus, DE gases slowed AV conduction and ventricular repolarization, decreased BP, increased HRV, and subsequently provoked arrhythmias, collectively suggesting parasympathetic activation; conversely, brief BP and HRV changes after exposure to particle-containing DE indicated a transient sympathetic excitation. Our findings suggest that whole- and particle-free DE differentially alter CV and autonomic physiology and may potentially increase risk through divergent pathways.