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A single exposure to acrolein desensitizes baroreflex responsiveness and increases cardiac arrhythmias in normotensive and hypertensive rats
Citation:
Hazari, M., J. Griggs, D. Winsett, N. Coates, A. Ledbetter, D. Costa, AND A. Farraj. A single exposure to acrolein desensitizes baroreflex responsiveness and increases cardiac arrhythmias in normotensive and hypertensive rats. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, 14(1):52-63, (2014).
Impact/Purpose:
This manuscript describes the effects of a single acrolein exposure on cardiovascular function in rats. It demonstrates that exposure to this hazardous air toxicant causes dysfunctional regulation of cardiovascular function and increased risk of arrhythmia. These data fulfill the Agency's mandate of studying the health effects of hazardous air pollutants and the risk they could potentially pose to susceptible populations.
Description:
Background – Short-term exposure to air pollutants has been linked to acute cardiovascular morbidity and mortality. Even in the absence of overt symptoms, pollutants can cause subtle disruptions of internal regulatory mechanisms, which maintain homeostatic balance, thereby reducing the body’s ability to compensate for various stressors and resulting in adverse responses. Objective – We hypothesized that a single exposure to acrolein, a ubiquitous gaseous air pollutant, would decrease the sensitivity of baroreflex (BRS), which maintains blood pressure by altering heart rate, and increase cardiac arrhythmogenesis in rats. Methods – Wistar-Kyoto normotensive (WKY) and Spontaneously Hypertensive (SH) rats implanted with radiotelemeters and a chronic intravenous catheter were exposed whole-body to 3ppm acrolein (3hrs). All animals were tested for BRS pharmacologically using phenylephrine (PE) and sodium nitroprusside (SNP) two days before and one hour after exposure. Heart rate (HR) and electrocardiogram (ECG) were continuously monitored in the pre-exposure, exposure and post-exposure periods. Results – Prior to exposure, SH rats already had significantly higher blood pressure, lower BRS and increased non-conducted p-wave arrhythmias when compared to WKY rats. A single exposure to acrolein caused a significant decrease in BRS and increased incidence of arrhythmia in both WKY and SH rats. There were minimal ECG differences between the strains whereas only SH rats experienced irregular breathing during acrolein. Conclusions – These results demonstrate that exposure to acrolein results in immediate cardiovascular reflexive dysfunction and persistent arrhythmia in both normal and hypertensive animals. As such, homeostatic imbalance may be one mechanism by which air pollution increases risk, particularly in people with underlying cardiovascular disease in the twenty-four hours following exposure.