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ToxSci Advance Access published online on August 10, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi283
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received May 17, 2005
Accepted July 23, 2005

Environmental Toxicology

Nonparticulate Components of Diesel Exhaust Promote Constriction in Coronary Arteries from ApoE-/- Mice

Matthew J. Campen 1*, N. Sathish Babu 2, G. Andrew Helms 2, Stuart Pett 2, Jorge Wernly 2, Reza Mehran 3, and Jacob D. McDonald 1

1 Department of Toxicology, Lovelace Respiratory Research Institute, Albuquerque, NM, 87108
2 Department of Cardiothoracic Surgery, University of New Mexico School of Medicine, Albuquerque, NM, 87131
3 Department of Surgery, M D Anderson School of Medicine, Houston, TX, 77030

* To whom correspondence should be addressed.
Matthew J. Campen, E-mail: mcampen{at}LRRI.org


  Abstract

Air pollution is positively associated with increased daily incidence of myocardial infarction and cardiovascular mortality. We hypothesize that air pollutants, primarily vapor phase organic compounds, cause an enhancement of coronary vascular constriction. Such events may predispose susceptible individuals to anginal symptoms and/or exacerbation of infarction. To develop this hypothesis, we studied the effects of nonparticulate diesel exhaust constituents on (1) electrocardiographic traces from ApoE-/- mice exposed whole-body and (2) isolated, pressurized septal coronary arteries from ApoE-/- mice. ApoE-/- mice were implanted with radiotelemetry devices to assess electrocardiogram (ECG) waveforms continuously throughout exposures (6 h/d x 3 d) to diesel exhaust (0.5 and 3.6 mg/m3) in whole-body inhalation chambers with or without particulates filtered. Significant bradycardia and T-wave depression were observed, regardless of the presence of particulates. Pulmonary inflammation was present only in the whole exhaust-exposed animals at the highest concentration. Fresh diesel exhaust or air was bubbled through the physiologic saline tissue bath prior to experiments to enable the isolated tissue exposure; exposed saline contained elevated levels of several volatile carbonyls and alkanes, but little to no polycyclic aromatic hydrocarbons. Vessels were then assayed for constrictive and dilatory function. Diesel components enhanced the vasoconstrictive effects of endothelin-1 and reduced the dilatory response to sodium nitroprusside. These data demonstrate that nonparticulate compounds in whole diesel exhaust elicit ECG changes consistent with myocardial ischemia. Furthermore, the volatile organic compounds in the vapor phase caused enhanced constriction and reduced dilatation in isolated coronary arteries caused by nonparticulate components of diesel exhaust.

Keywords: ischemia; vasospasm; air pollution; particulate matter; volatile organic compounds.
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