Rats exposed to wDE developed arrhythmia at lower doses of aconitine than did controls; the dose was even lower in rats exposed to fDE.
It is believed that blockade of this receptor would prevent activation of airway sensory nerves and the autonomic reflex arc and would thus prevent the heightened response to aconitine by severing the outgoing signal that connects the autonomic nervous system to the heart.
HR and ECG waveforms were continuously acquired and saved during the 5-min baseline period and aconitine challenge.
Arrhythmias were identified as occurring sequentially during aconitine challenge as ventricular premature beats (VPBs), ventricular tachycardia (VT), and ventricular fibrillation (VF) [see Supplemental Material, Figure 1 (doi:10.
Animals received bilateral vagotomy, the sympathetic adrenergic blocker guanethidine, or the muscarinic (parasympathetic) antagonist atropine after exposure to either FA or wDE (30 min before aconitine challenge).
Stock solutions of aconitine (Sigma-Aldrich) were dissolved in ethanol and then diluted to the desired concentration with saline.
All aconitine dose-response data were analyzed using an analysis of variance for repeated measures; p < 0.
Figure 2 shows the responses to aconitine in the low wDE and TRP experiments.
Treatment with the sympathetic blocker guanethidine before aconitine challenge prevented the potentiated arrhythmic response to aconitine and significantly increased the dose necessary to cause cardiac arrest in low wDE-exposed rats; it had no effect on controls (Figure 3A).