Pharmacologic evidence for a parasympathetic role in seizure-induced neurocardiac regulatory abnormalities.

Abstract

PURPOSE: We evaluated whether postictal cardiac arrhythmia can be prevented by pharmacologic blockage of peripheral muscarinic receptors in an experimental model of epilepsy in rats. METHODS: Rats were prepared for chronic electrocardiograph recording and pretreated with atropine methyl bromide (2 or 10mg/kg i.p.) or saline prior to exposure to maximal electroshock (MES). The resulting seizure severity and duration of cardiac arrhythmia were measured. RESULTS: Atropine methyl bromide did not significantly affect seizure severity in comparison to control animals but reduced the arrhythmia at a dose of 2mg/kg, and completely suppressed arrhythmia at 10mg/kg. CONCLUSIONS: Postictal arrhythmia following MES-induced seizures may be blocked by pretreatment with atropine methyl bromide, a peripherally acting parasympatholytic agent. Our findings support previous observations that suggest strong participation of the parasympathetic system in postictal arrhythmia. This may be important for clinical suppression of cardiac arrhythmia in persons with uncontrolled epilepsy, who are at risk for sudden unexpected death.