Key result
Acute toluene exposure increased perfusion pressure, left ventricular developed pressure, and heart rate in rats, and these actions were inhibited by lidocaine and nifedipine.
Toluene cardiotoxicity may involve sodium channels; hypothesis-generating for lidocaine in solvent-induced arrhythmias.
Inhaling solvents can lead to occurrence of cardiac arrhythmias and sudden sniffing death. Mechanisms related to this phenomenon are not fully understood. The purpose of this study was to investigate the effect of acute toluene exposure on heart reactivity to epinephrine and the participation of voltage-gated sodium and calcium channels. We found that acute toluene exposure increased perfusion pressure, left ventricular developed pressure, and heart rate. These actions were inhibited by lidocaine and nifedipine. Our results suggest that acute toluene exposure modify voltage-gated sodium and calcium channel function and expression likely due to a cardiac adrenergic mechanism and these effects could be participating, at least in part, in the presence of cardiac arrhythmias. To our best knowledge, this is the first report to establish a direct participation of voltage-gated Na+ and Ca2+ channels, toluene and epinephrine on cardiac function in rats.
No takes yet. Share an insight, caveat, or question.
Carreón-Garcidueñas et al. (2018) studied Cardiac arrhythmias and sudden sniffing death related to solvent inhalation. Acute toluene exposure was evaluated on Perfusion pressure, left ventricular developed pressure, and heart rate. Acute toluene exposure increased perfusion pressure, left ventricular developed pressure, and heart rate in rats, and these actions were inhibited by lidocaine and nifedipine.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: