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A single inhalation exposure to acrolein desensitizes baroreflex responsiveness in Wistar-Kyoto and Spontaneously Hypertensive rats.
HAZARI, M. S., K. Butler, D. W. WINSETT, D. L. Costa, AND A. FARRAJ. A single inhalation exposure to acrolein desensitizes baroreflex responsiveness in Wistar-Kyoto and Spontaneously Hypertensive rats. Presented at Society of Toxicology (SOT) Annual Meeting, San Francisco, CA, March 11 - 15, 2012.
This study describes the effects of a single exposure to acrolein on baroreflex sensitivity (BRS) in Wi star-Kyoto and spontaneously hypertensive rats. Acrolein inhalation desensitized BRS and increased cardiac arrhythmias in both strains of rat.
Arterial baroreflex is one of the body's homeostatic mechanisms that regulate blood pressure (BP) by changing heart rate (HR) and vasoconstriction. Increases in BP reflexively cause HR to decrease, whereas decreases in BP depress the baroreflex and cause HR to rise. As such, baroreflex sensitivity (BRS) is often used as a predictor of impaired autonomic control and cardiovascular disease, and has been found to be reduced in various cardiovascular conditions such as chronic heart failure, post-infarction and hypertension. Given air pollution can alter autonomic balance, we hypothesized that exposure to air pollutants would also alter BRS and increase the risk ofadverse cardiovascular events. Conscious unrestrained Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rats implanted with an intravenous catheter and radiotelemeters were administered increasing doses of phenylephrine (PE-vasoconstrictor) and then sodium nitroprusside (SNP-vasodilator) while HR response, BP, and electrocardiogram (ECG) were continuously measured. This BRS test was done one day before and one day after exposure to either air or 3ppm acrolein (3hrs). Before exposure, PE caused a dose-dependent increase in BP, which resulted in decreasing HR in WKY rats; SNP caused a dose-dependent decrease in BP and resulting HR increases. SH rats had a similar BRS response; however, the reflexive changes in HR due to BP increase/decrease were attenuated at the higher doses. Twenty-four hours after acrolein, BRS was decreased in WKY rats and further blunted in SH rats. SH rats had significantly more arrhythmias than WKY rats during and after exposure to acrolein. Although SH rats had higher baseline BP, there were no other ECG differences between strains. In conclusion, a single exposure to a toxic air pollutant alters the body's ability to reflexively regulate cardiovascular function and predisposes to adverse cardiac events. (This abstract does not reflect EPA policy)