ToxSci Advance Access originally published online on May 12, 2004
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Toxicological Sciences 80, 367-376 (2004)
Toxicological Sciences vol. 80 no. 2 © Society of Toxicology 2004; all rights reserved.
Cardiac Effects of Carbon Monoxide and Ambient Particles in a Rat Model of Myocardial Infarction
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* Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115; Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts 02115; Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215; and Harvard Medical School, Boston, Massachusetts 02115
Received February 19, 2004; accepted April 29, 2004
Ambient air pollution is a complex mixture of particulate matter (PM) and gaseous pollutants such as carbon monoxide (CO). The effect of exposure to CO, alone or in combination with ambient PM, on arrhythmia incidence is unclear. To evaluate these effects, left-ventricular myocardial infarction was induced in Sprague-Dawley rats by thermocoagulation. Diazepam-sedated rats were exposed (1 h) to either filtered air (n = 40), CO (35 ppm, n = 19), concentrated air particles (CAPs, median concentration = 350.5 µg/m3, n = 53), or CAPs and CO (CAPs median concentration = 318.2 µg/m3, n = 23), 12–18 h after surgery. Each exposure was immediately preceded and followed by a 1 h exposure to filtered air (pre-exposure and post-exposure periods, respectively). The CO target dose of 35 ppm is related to the 1 h U.S. National Ambient Air Quality Standard. Surface electrocardiograms were recorded and heart rate and arrhythmia incidence were quantified. CO exposure reduced ventricular premature beat (VPB) frequency by 60.4% (p = 0.012) during the exposure period compared to controls. This effect was modified by both infarct type and the number of pre-exposure VPBs, and was not mediated through changes in heart rate. Overall, CAPs exposure increased VPB frequency during the exposure period, but this effect did not reach statistical significance. This effect was modified by the number of pre-exposure VPBs. Overall, neither CAPs nor CO had any effect on heart rate, but CAPs increased heart rate in specific subgroups. No significant interactions were observed between the effects of CO and CAPs. In this animal model, the responses to CO and CAPs are distinctly different.
Key Words: arrhythmia; myocardial infarction; carbon monoxide; particulate matter; air pollution; cardiovascular; Sprague-Dawley rats.
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