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Simultaneous exposure to concentrated ambient particles and acrolein causes cardiac effects mediated by parasympathetic modulation in mice
Citation:
Kurhanewicz, N., A. Ledbetter, L. Walsh, A. Farraj, AND M. Hazari. Simultaneous exposure to concentrated ambient particles and acrolein causes cardiac effects mediated by parasympathetic modulation in mice. Society of Toxicology 2016, New Orleans, LA, March 14 - 17, 2016.
Impact/Purpose:
Determine the effect of simultaneous exposure to concentrated ambient particles and acrolein on cardiovascular parameters in mice
Description:
This study shows that exposure to CAPs and acrolein causes an increase in HRV that is mediated by the parasympathetic nervous system. Numerous studies show that short-term air pollution exposure modulates heart rate variability (HRV), which is an indicator of autonomic influence on the heart and measure of cardiovascular homeostatic control and risk. Our previous studies show that a single exposure to air pollution increases arrhythmia in mice in a manner that implicates autonomic imbalance. Thus, the goal of this study was to characterize the autonomic changes due to exposure as reflected by HRV. We hypothesized that pharmacological inhibition of the parasympathetic and sympathetic effects on the heart would block the cardiac response to air pollution. Conscious, unrestrained C57BL/6 mice were exposed to ~40 ug/m3 concentrated ambient particles (CAPs) and 0.3 ppm acrolein for 3 hours. Immediately prior to exposure separate cohorts were treated with either atropine (2 mg/kg) or atenolol (2 mg/kg) to block the parasympathetic or sympathetic influence on the heart, respectively, hexamethonium (80 mg/kg) to block both, or saline. Electrocardiogram (ECG) and HR were recorded continuously before, during and after exposure. Treatment with atropine and hex increased HR and decreased HRV whereas atenolol did the opposite. Exposure to CAPs+acrolein did not affect HR, however SDNN and RMSSD both increased when compared with filtered air exposure. Pretreatment with both atropine and hex blocked this response whereas atenolol had no effect. Thus inhibition of parasympathetic influence blocked the HRV response (and arrhythmia) to air pollution exposure. These data demonstrate that even low level exposures to air pollution, which may not cause observable symptoms, can disrupt normal autonomic balance in healthy young animals and that these changes are characterized by parasympathetic dominance. (This abstract does not reflect USEPA policy)