A Single Exposure to Particulate or Gaseous Air Pollution Increases the Risk of Aconitine-Induced Cardiac Arrhythmia in Hypertensive Rats
A Single Exposure to Particulate or Gaseous Air Pollution Increases the Risk of Aconitine-Induced Cardiac Arrhythmia in Hypertensive Rats
复制标题
DOI：
10.1093/toxsci/kfp214
复制
发表时间：
2009-12-01
影响因子：
3.8
通讯作者：
Farraj, Aimen K.
中科院分区：
文献类型：
--
作者：
Hazari, Mehdi S.;Haykal-Coates, Najwa;Farraj, Aimen K.
流行病学研究表明心律失常与空气污染之间存在关联。乌头碱引起的心律失常被广泛用于实验研究改变心律失常发生风险的因素。在这项研究中，Wistar-Kyoto （WKY）和自发性高血压（SH）大鼠急性暴露于合成残油飞灰（s-ROFA）颗粒（450 μ g/m(3)），用乌头碱“刺激”，以检查单次暴露是否会诱发心律失常。另外，SH大鼠暴露于不同浓度的颗粒物（PM）（0.45、1.0或3.5 mg/m(3) s-ROFA）或刺激性气体丙烯醛（3ppm），以更好地评估这种挑战反应的泛化性。而不是直接导致心律失常，我们假设吸入的空气污染物使心脏对随后的心律失常刺激敏感。暴露24小时后，监测尿素麻醉大鼠心率（HR）、心电图和血压（BP）。SH大鼠的基线HR和BP均高于WKY大鼠，PR间隔、QRS持续时间、QTc和JTc均显著长于WKY大鼠。PM暴露导致WKY大鼠PR间隔、QRS持续时间和QTc显著增加，而SH大鼠无明显增加。PM暴露后，WKY大鼠心率变异性显著降低，SH大鼠心率变异性增加。暴露于空气中的SH大鼠引起心律失常的乌头碱累积剂量低于WKY大鼠，各品系暴露后的乌头碱累积剂量甚至更低。暴露于不同浓度的PM或丙烯醛的SH大鼠在乌头碱剂量显著低于对照组时出现心律失常；然而，没有PM浓度依赖性的反应。总之，单次暴露于空气污染可能会增加心脏电传导对中断的敏感性。此外，似乎存在宿主因素（如心血管疾病），无论污染物或其浓度如何，都增加了诱发心律失常的易感性。
Epidemiological studies demonstrate an association between arrhythmias and air pollution. Aconitine-induced cardiac arrhythmia is widely used experimentally to examine factors that alter the risk of arrhythmogenesis. In this study, Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rats acutely exposed to synthetic residual oil fly ash (s-ROFA) particles (450 mu g/m(3)) were "challenged" with aconitine to examine whether a single exposure could predispose to arrhythmogenesis. Separately, SH rats were exposed to varied particulate matter (PM) concentrations (0.45, 1.0, or 3.5 mg/m(3) s-ROFA), or the irritant gas acrolein (3 ppm), to better assess the generalization of this challenge response. Rather than directly cause arrhythmias, we hypothesized that inhaled air pollutants sensitize the heart to subsequent dysrhythmic stimuli. Twenty-four hour postexposure, urethane-anesthetized rats were monitored for heart rate (HR), electrocardiogram, and blood pressure (BP). SH rats had higher baseline HR and BP and significantly longer PR intervals, QRS duration, QTc, and JTc than WKY rats. PM exposure caused a significant increase in the PR interval, QRS duration, and QTc in WKY rats but not in SH rats. Heart rate variability was significantly decreased in WKY rats after PM exposure but increased in SH rats. Cumulative dose of aconitine that triggered arrhythmias in air-exposed SH rats was lower than WKY rats and even lower for each strain postexposure. SH rats exposed to varied concentrations of PM or acrolein developed arrhythmia at significantly lower doses of aconitine than controls; however, there was no PM concentration-dependent response. In conclusion, a single exposure to air pollution may increase the sensitivity of cardiac electrical conduction to disruption. Moreover, there seem to be host factors (e.g., cardiovascular disease) that increase vulnerability to triggered arrhythmias regardless of the pollutant or its concentration.