Epidemiological studies demonstrate a significant association between arrhythmias and air pollution exposure. Sensitivity to aconitine-induced arrhythmia has been employed to examine the factors that increase the risk of such dysfunction. We used aconitine to test whether a single exposure to diesel exhaust (DE) would increase the risk of arrhythmia being triggered in hypertensive rats. We hypothesised that DE exposure increases the risk of arrhythmia due to sensory irritation during and after inhalation. Spontaneously hypertensive rats surgically implanted with radiotelemeters were exposed to 150 μg/m3 of DE or filtered air for 4 h. Arrhythmogenesis was assessed 24 h later in urethane-anaesthetised animals by continuous intravenous infusion of aconitine while heart rate (HR) and electrocardiogram (ECG) were monitored. Rats exposed to DE had lower HR when compared to air-exposed animals. Exposure to DE resulted in significantly shorter PR intervals, and significantly prolonged corrected QT (QTc) and corrected JT (JTc) when compared to air exposure. 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 DE successively developed VPB's, VT, and VF at significantly lower doses of aconitine than air-exposed animals. Pre-exposure treatment of rats exposed to DE with a transient receptor potential A1 (TRPA1) antagonist prevented the heightened sensitivity to aconitine-induced arrhythmia. These findings suggest that a single exposure to DE increases arrhythmogenic sensitivity. This heightened sensitivity may be mediated by activation of TRPA1 on airway sensory nerves, which are particularly sensitive to inhaled irritants. (This abstract does not reflect EPA policy.)
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