Diesel Exhaust Inhalation Increases Cardiac Output, Bradyarrhythmias, and Parasympathetic Tone in Aged Heart Failure-Prone Rats
Diesel Exhaust Inhalation Increases Cardiac Output, Bradyarrhythmias, and Parasympathetic Tone in Aged Heart Failure-Prone Rats
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DOI：
10.1093/toxsci/kfs295
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发表时间：
2013-02-01
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.;Lust, Robert M.;Farraj, Aimen K.
急性空气污染物吸入与不良心脏事件和死亡以及心力衰竭住院有关。柴油发动机排气（DE）是一种主要的空气污染物，被怀疑会加重先前存在的心脏疾病，部分原因是通过正常心脏功能的自主神经和电生理紊乱。为了探讨这一假定的机制，我们在一个没有明显心力衰竭体征或症状的老年心力衰竭易感大鼠模型中检测了吸入DE的心脏生理反应。我们假设急性DE暴露会改变心律、心脏电生理学和心室性能以及与自主神经失衡一致的尺寸，同时增加毒性的生化标志物。将自发性高血压心力衰竭大鼠（16个月）暴露于全DE（4小时，目标PM2.5浓度：500 g/m3）或过滤空气中一次。暴露期间，DE增加了多个心率变异性（HRV）参数。暴露后4小时，DE增加心输出量、左心室容积（舒张末期和收缩末期）、每搏输出量、HRV和房室阻滞性心律失常，同时增加心室复极的心电图测量（即，ST和T振幅、ST面积、T峰至T结束持续时间）。相对于空气，DE不影响心率。心率变异性的变化与缓慢性心律失常频率、复极和超声心动图参数的变化呈正相关。在24小时后，DE暴露大鼠血清C-反应蛋白和肺嗜酸性粒细胞增加。这项研究表明，DE吸入的心脏影响可能会发生通过与心脏电生理和机械功能的调制相关的自主平衡的变化，并可能提供洞察交通相关的空气污染物的不良健康影响。
Acute air pollutant inhalation is linked to adverse cardiac events and death, and hospitalizations for heart failure. Diesel engine exhaust (DE) is a major air pollutant suspected to exacerbate preexisting cardiac conditions, in part, through autonomic and electrophysiologic disturbance of normal cardiac function. To explore this putative mechanism, we examined cardiophysiologic responses to DE inhalation in a model of aged heart failureprone rats without signs or symptoms of overt heart failure. We hypothesized that acute DE exposure would alter heart rhythm, cardiac electrophysiology, and ventricular performance and dimensions consistent with autonomic imbalance while increasing biochemical markers of toxicity. Spontaneously hypertensive heart failure rats (16 months) were exposed once to whole DE (4h, target PM2.5 concentration: 500 g/m(3)) or filtered air. DE increased multiple heart rate variability (HRV) parameters during exposure. In the 4h after exposure, DE increased cardiac output, left ventricular volume (end diastolic and systolic), stroke volume, HRV, and atrioventricular block arrhythmias while increasing electrocardiographic measures of ventricular repolarization (i.e., ST and T amplitudes, ST area, T-peak to T-end duration). DE did not affect heart rate relative to air. Changes in HRV positively correlated with postexposure changes in bradyarrhythmia frequency, repolarization, and echocardiographic parameters. At 24h postexposure, DE-exposed rats had increased serum C-reactive protein and pulmonary eosinophils. This study demonstrates that cardiac effects of DE inhalation are likely to occur through changes in autonomic balance associated with modulation of cardiac electrophysiology and mechanical function and may offer insights into the adverse health effects of traffic-related air pollutants.