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Aconitine Challenge Test Reveals a Single Exposure to Air Pollution Causes Increased Cardiac Arrhythmia Risk in Hypertensive Rats - Abstract
Citation:
HAZARI, M. S., N. HAYKAL-COATES, D. W. WINSETT, D. L. COSTA, AND A. FARRAJ. Aconitine Challenge Test Reveals a Single Exposure to Air Pollution Causes Increased Cardiac Arrhythmia Risk in Hypertensive Rats - Abstract. Presented at 2009 Annual Society of Toxicology meeting , Baltimore, MD, March 15 - 19, 2009.
Impact/Purpose:
This study describes the effects of a single exposure to residual oil fly ash (ROFA) or acrolein on aconitine-induced arrhythmogenicity in spontaneously hypertensive (SH) rats. A lower cumulative dose of aconitine was needed to elicit arrhythmia in rats exposed to ROFA when compared to air-exposed controls.
Description:
Epidemiological studies demonstrate a significant association between arrhythmias and air pollution exposure. Sensitivity to aconitine-induced arrhythmia has been used repeatedly to examine the factors that increase the risk of such cardiac electrical dysfunction. In this study, we are the first to use a technique known to elicit arrhythmia to examine whether inhalation exposure to particulate air pollutants or gaseous irritants increases the risk of arrhythmia being triggered in a rat model of hypertension. Spontaneously hypertensive rats implanted with radiotelemeters were exposed for 3 hours to 3mg/m3 (high), 1mg/m3 (med) or 0.45mg/m3 (low) metal-rich synthetic residual oil fly ash (s-ROFA), 3ppm acrolein, or filtered air. Arrhythmogenesis was assessed 24 hours later in urethane-anesthetized animals by continuous intravenous infusion of aconitine while heart rate, ECG and ventilatory parameters were monitored. Sensitivity to arrhythmia was measured as the threshold dose of aconitine required to produce ventricular premature beats (VPB), ventricular tachycardia (VT), and ventricular fibrillation (VF). Rats exposed to filtered air developed VPB’s, VT, and VF successively during aconitine infusion. Rats exposed to low, med and high s-ROFA, and acrolein developed VPB’s, VT, and VF at significantly lower doses of aconitine than air-exposed animals. The cumulative dose of aconitine required to elicit these responses was lowest in animals exposed to acrolein followed by high s-ROFA. Paradoxically, arrhythmia was elicited at lower doses of aconitine in low s-ROFA-exposed animals than med. S-ROFA. These findings suggest that a single exposure to a toxic air pollutant, whether particulate or gaseous, can increase the sensitivity of the cardiac electrical conduction system and trigger arrhythmia; which poses a particular health risk to individuals with cardiovascular disease.