Many clinical cases have been reported where epilepsy profoundly influenced the 
pathophysiological function of the heart; however, the underlying mechanisms 
were not elucidated. We use the tremor (TRM) rat as an animal model of epilepsy 
to investigate the potential mechanisms of myocardial injury. Cardiac functions 
were assessed by arrhythmia score, heart rate, heart:body mass ratio, and 
hemodynamic parameters including left ventricular systolic pressure (LVSP), left 
ventricular end-diastolic pressure (LVEDP), and maximum rate of left ventricular 
pressure rise and fall (+dp/dtmax and -dp/dtmax). Catecholamine level was 
detected by HPLC. Apoptotic index was estimated by TUNEL assay. The expressions 
of Bcl-2, Bax, caspase-3, extracellular signal-regulated protein kinase (ERK), 
c-Jun NH2-terminal protein kinases (JNK), and p38 were evaluated by Western 
blot. The results indicated that there existed cardiac dysfunction and 
cardiomyocyte apoptosis, accompanied by increasing catecholamine levels in TRM 
rats. Further investigation revealed that apoptosis was mediated by reducing 
Bcl-2, upregulating Bax, and activating caspase-3. Additional experiments 
demonstrated that P-ERK1/2 was decreased, whereas P-JNK and P-p38 were 
up-regulated. Our results suggest that the sympathetic nervous system activation 
and cardiomyocyte apoptosis are involved in the myocardial injury of TRM rats. 
The mechanisms of apoptosis might be associated with the activation of the 
mitochondria-initiated and the mitogen-activated protein kinase pathways.