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Particles Alter Diesel Exhaust Gases-Induced Hypotension, Cardiac Arrhythmia,Conduction Disturbance, and Autonomic Imbalance in Heart Failure-Prone Rats
Citation:
Carll, A. P., M. S. HAZARI, C. M. Perez, Q. T. KRANTZ, C. KING, D. W. WINSETT, D. L. Costa, AND A. FARRAJ. Particles Alter Diesel Exhaust Gases-Induced Hypotension, Cardiac Arrhythmia,Conduction Disturbance, and Autonomic Imbalance in Heart Failure-Prone Rats. Presented at American Thoracic Society (ATS) Meeting, San Francisco, CA, May 18 - 23, 2012.
Impact/Purpose:
We demonstrate that acute exposure to DE gases slowed AV conduction and ventricular repolarization and provoked a proarrhythmic vagal dominance that was attenuated with the inclusion of DE particles. Our findings demonstrate that the gaseous and particulate components of DE can disparately affect cardiovascular physiology and autonomic balance.
Description:
Epidemiologic studies indicate that acute exposures to vehicular traffic and particulate matter (PM) air pollution are key causes of fatal cardiac arrhythmia, especially in those with preexisting cardiovascular disease. Researchers point to electrophysiologic dysfunction and autonomic imbalance as major mechanisms mediating this cardiac toxicity. Diesel engine exhaust (DE) is a major contributor to urban ambient PM and gaseous pollutants. To determine the role of DE's gaseous and particulate components in air pollutant cardiotoxicity, we examined the effects of a 4-hourwhole-body inhalation of whole DE(wDE; target PM concentration: 500 ug/m3) or particle-free filtered DE (fDE) on cardiovascular physiology and biochemistry in hypertensive heart failure-prone rats. Arterial blood pressure (BP), electrocardiography (ECG), and heart rate variability (HRV, an index of autonomic balance) were monitored. During exposure, DE gases caused physiologic changes consistent with parasympathetic dominance, as both fDE and wDE decreased BP and prolonged PR interval, with more pronounced effects from fDE, which also increased HRV triangular index and decreased T-wave amplitude (P<.05). Immediately after exposure, fDE increased QTc interval, while wDE appeared to elicit sympathetic dominance, marked by increased BP and decreased HRV root mean square of successive differences (P<.05). During the six hours following exposure, ,fDE increased Mobitz II atrioventricular (AV) block arrhythmias and high-density lipoprotein (p<.05), while both fDE and wDE transiently decreased heart rate and low-to-high frequency ratio o fHRV. Thus, acute exposure to DE gases slowed AV conduction and ventricular repolarization, provoked parasympathetic dominance, and caused cardiac arrhythmia, while inclusion of DE particles attenuated these effects with evidence sympathetic excitation. Our findings suggest that, through disparate effects on autonomic balance, the gaseous and particulate components of DE differentially compromise cardiovascular physiology, leading to divergent outcomes