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DIFFERENTIAL CARDIAC ARRHYTHMIA PROFILES IN HYPERTENSIVE AND NORMAL RATS AFTER EMISSION SOURCE PARTICULATE EXPOSURE
Citation:
FARRAJ, A., D. W. WINSETT, N. HAYKAL-COATES, M. S. HAZARI, A. P. CARLL, A. D. LEDBETTER, AND D. L. COSTA. DIFFERENTIAL CARDIAC ARRHYTHMIA PROFILES IN HYPERTENSIVE AND NORMAL RATS AFTER EMISSION SOURCE PARTICULATE EXPOSURE . Presented at Society of Toxicology Annual Meeting, Seattle, WA, March 16 - 20, 2008.
Impact/Purpose:
We tested the hypothesis that the Spontaneously Hypertensive (SH) rat, a hypertension-prone strain, will be more susceptible to the development of PM-induced arrhythmia than its corresponding normotensive background control, the Wistar Kyoto (WKY) rat.
Description:
Exposure to combustion-derived fine particulate air pollution is associated with increased cardiovascular morbidity and mortality. These effects are especially conspicuous in individuals with pre-existing cardiovascular diseases including hypertension and coronary heart disease. PM exposure causes altered cardiac rhythm often manifested as ST depression, altered ventricular repolarization, and reduced heart rate variability. There are currently no widely-accepted mechanisms of action of particulate-induced exacerbation of cardiovascular disease especially at ambient levels of exposure. In addition, few rodent models have reproduced the PM-induced dysrhythmias observed in susceptible humans. We tested the hypothesis that the Spontaneously Hypertensive (SH) rat, a hypertension-prone strain, will be more susceptible to the development of PM-induced arrhythmia than its corresponding normotensive background control, the Wistar Kyoto (WKY) rat. Rats were exposed once via inhalation (nose-only) for 4 hours to residual oil fly ash (ROFA), an emission source particle rich in transition metals, or air, and then sacrificed 1 or 48 h post exposure. SH rats exposed to ROFA had greater pulmonary injury, greater neutrophil infiltration into the lungs, and higher levels of the serum acute-phase marker C-reactive protein than similarly exposed WKY rats 48 h post exposure. In addition, only the ROFA-exposed SH rats had shorter ST, QT, and RR interval length relative to air exposed animals during exposure, suggesting that the hypertensive state may result in proarrhythmogenic changes in the myocardium of the SH rats. Interestingly, ROFA exposure in the WKY rats but not SH rats caused a reduction in the low frequency (LF) power spectra, a measure of heart rate variability that reflects sympathetic tone. Taken together, these results suggest that ROFA exposure exacerbates myocardial vulnerability in SH rats while causing some level of autonomic dysregulation in WKY rats (This abstract does not reflect EPA policy; funded in part by EPA CT82947101 and T32-ES07126).