Objective      To investigate the cardioprotective effect of p-nitro caffeic acid phenethyl ester (CAPE-NO

2

)

which is synthesized by coupling nitro group to CAPE

on isoproterenol (ISO)-induced myocardial infarction in rats and its underlying mechanisms.       Methods      Ma

le Sprague-Dawley rats were randomly divided into 5 groups: Control group

CAPE-NO

2

group

ISO group

CAPE+ISO group and CAPE-NO

2

+ISO group. CAPE (50 μg/kg) and CAPE-NO

2

(50 μg/kg) were injected intraperitoneally into the rats for 7 d

and then the rats were administered with ISO (85 mg/kg) subcutaneously to induce myocardial injury. After that

the rats were anaesthetized with pentobarbital sodium (40 mg/kg) to record electrocardiogram

and then sacrificed to detect the infarct size and biochemical indexes of the heart tissues.       Results      The rats treated with ISO showed marked elevation in ST-segment (P0.05)

enlargement in QRS duration (P0.05)

significant increase in the infarct size (P0.01) and NO content (P0.01)

and significant decrease in the activities of endogenous antioxidants (SOD

CAT and GSH-Px) (P0.01). Compared with the ISO group

both the CAPE+ ISO group and the CAPE-NO

2

+ISO group could significantly reduce the elevation of ST-segment (P0.05 and P0.01)

enlargement of QRS duration (P0.05)

infarct size (P0.05 and P0.01) and NO content (P0.05 and P0.01)

however

the effect of CAPE-NO

2

was more significant than that of CAPE. CAPE had no effect on the antioxidants

but the administration of CAPE-NO

2

resulted in significant rise of the antioxidants activities.       Conclusion      The cardioprotective effect of CAPE-NO

2

on ISO-induced myocardial infarction is better than that of CAPE in the rats. The mechanism might be associated with the elevation of antioxidant activity to inhibit oxidative stress and nitrative stress.