AIM: To observe the myocardial protective effects of trimetazidine on myocardial infarction(MI) in Sprague-Dawley(SD) rats.METHODS: Ninety SD rats were randomly assigned to 3 groups(n=30 each): myocardial infarction group(MI group),MI+trimetazidine group(MT group) and sham group(S group).By permanently ligating the left anterior descending artery,the MI model was set up in the rats in MI group and MT group.Before and after setting up the MI model,normal saline was given to the rats in MI and S group by gavage.On the other hand,trimetazidine(3 mg/kg,twice per day) was given to the rats in MT group by gavage.At 8 h,24 h and 48 h after applying trimetazidine,the serum level of cardiac troponin I(cTnI) was measured.At the 1st week,2nd week and 4th week after treated with trimetazidine,the size of myocardial infarction,the maximum rising rate of the left ventricular systolic pressure(+dp/dtmax) and the maximum descending rate of the left ventricular diastolic pressure(-dp/dtmax) were measured.Also at the 1st week after applying trimetazidine,the cardiomyocyte apoptotic index was detected.RESULTS: Compared with MI group 2 weeks after applying trimetazidine,+dp/dtmax significantly increased in MT group [(8 101±990) mmHg/s vs(5 868±1 302) mmHg/s,P0.01],and-dp/dtmax also significantly increased in MT group [(6 514±1 558) mmHg/s vs(4 750±1 463) mmHg/s,P0.01].Four weeks after applying trimetazidine,+dp/dtmax significantly increased in MT group [(7 629±1 181) mmHg/s vs(5 620±454) mmHg/s,P0.01],and-dp/dtmax also significantly increased in MT group [(5 883±1 379) mmHg/s vs(4 256±731) mmHg/s,P0.01].At 8 h and 48 h after applying trimetazidine,no statistically significant difference(P0.05) of serum cTnI between MI group and MT group was observed.However,at 24 h after applying trimetazidine,the serum level of cTnI decreased in MT group [(22.7±14.9) μg/L] as compared with MI group [(42.3±16.2) μg/L,P0.01].Aditionally,trimetazidine significantly decreased the infarction size of myocardium in MT group(0.248±0.052) as compared with MI group(0.362±0.082,P0.01).CONCLUSION: Trimetazidine has short-term cardioprotective effects on the rats with acute MI by improving myocardial systolic and diastolic functions,reducing infarct size and inhibiting apoptosis.

Objective To observe the myocardial protection effects of trimetazidine on Sprague-Dawley (SD) rats with myocardial infarctions (MI). Methods 90 SD rats were randomly assigned to normal control group (NL, n=30), Trimetazidine group (T, n=30) and sham-operated group (S, n=30). The MI model was set up in SD rats by permanent ligation of the left anterior descending coronary artery. In S group suture was through the left anterior descending coronary artery without ligation. Before and after MI, in NL group/S group and T group normal saline and Trimetazidine (0.3 mg/kg) were separately given by gavage. The changes of serum cTnI were observed at 8, 24, 48 h after MI. The changes of serum cTnI in S group was only observed at 24th hour after operations. In 1 week, 2 weeks and 4 weeks after treatment, the areas of myocardial infarction were analysed, and isovolumic systolic left ventricular maximum rate of pressure rise (+dp/dtmax) and isovolumic diastolic left ventricular maximum rate of pressure drop (−dp/dtmin) were measured to evaluate the myocardial protection effects of STV-1Na. The groups were compared with one-way analysis of variance (ANOVA) test. A value of p 0.05 between NL group and T group. But the serum cTnI level at 24 h after MI decreased in T group (22.7±5.3 ng/ml, p<0.05) compared with NL group (42.3±5.4 ng/ml). The serum cTnI level at 24 h in NL group and T group was significantly increased compared with S group (1.59±1.42 ng/ml) (p<0.01). Trimetazidine (0.248±0.021, p<0.01) decreased significantly the myocardial infarction area compared with NL group (0.362±0.027). The infarction areas in NL group (0.362±0.027) and T group (0.248±0.021) increased significantly compared with S group (0.072±0.1445) (p<0.01). In 1 week after MI, the +dp/dtmax in T group (7535±265) was not significantly different (p>0.05) compared with NL group (6702±329), and the -dp/dtmin in T group (−5511±400) was no significant difference (p>0.05) compared with NL group (−5400±339). In 2 weeks after MI, the +dp/dtmax in T group (8101±313) increased significantly compared with NL group (5868±412) (p<0.01), and the −dp/dtmin in T group (−6514±493) decreased significantly compared with NL group (−4750±463) (p<0.05). In 4 weeks after MI, in T group (7629±374) the +dp/dt max increased significantly compared with NL group (5876±200) (p<0.01,), and the −dp/dtmin in T group (−5883±436) decreased significantly compared with NL group (−4546±279) (p<0.05). The -dp/dt max in T group and NL group were significantly decreased (p<0.05) compared with S group in 1 week, 2 weeks and 4 weeks after the operation. The+dp/dtmin in T group and NL group were increased (p<0.05) compared to S group in 1 week, 2 weeks and 4 weeks after the operation. Conclusions Trimetazidine has myocardial protection effects on myocardial infarction and improves myocardial systolic and diastolic function in SD rats with acute myocardial infarction.