The aim of the present study was to investigate the protective effect of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino)
propane hydrochloride (
DDPH) on
myocardial ischemia-reperfusion (I/R) injury in rats and the mechanism of its myocardial protection. For this purpose, 50 Wistar rats were divided into five groups:
sham group, control group,
verapamil treated group, and two
DDPH treated groups (20 and 40 mg/kg, respectively). Myocardial I/R injury model was established by reperfusion for 120 min after 40 min
ischemia induced by the
ligation of left descending coronary artery in rats. The influence of
DDPH on
myocardial infarction size was observed and the levels of myocardial
enzymes in serum were measured. The activities of
oxygen free radical scavenging
enzymes and the content of
malondialdehyde (MDA) in myocardium and serum were determined. The pathological changes of myocardial tissue were observed. The results showed that
DDPH significantly diminished
myocardial infarction size, reduced the release of myocardial
creatine phosphokinase (CPK),
lactate dehydrogenase (LDH) and glutamic oxaloacetic
aminotransferase (GOT), protected the activities of
superoxide dismutase (SOD) and
glutathione peroxidase (GSH-Px), and decreased the content of MDA in myocardium and serum as compared with the control group. The degree of myocardial injury was slighter in
DDPH treated groups than in control group. These results suggest that
DDPH produces a cardioprotective effect during myocardial I/R injury, which may be related to blocking
calcium channels and inhibiting the formation of the
oxygen free radical and subsequent peroxidation of
lipid by
DDPH.