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目的 探讨曲美它嗪 (TMZ)对心肌缺血挛缩的保护作用。方法 大鼠分为A、B、C、D4组 ,A为对照组 ,微流量灌注 (0～ 1ml/min)制成心肌缺血模型 ,实验前口服曲美它嗪 (3mg/d× 7d) ,灌流液中加入 1× 10 -6mol/L的TMZ ,观察缺血后心脏发展压力的变化。结果 口服曲美它嗪、灌流液中添加曲美它嗪组与对照组相比 ,心肌缺血后发展压力有明显改善。缺血 30min时 ,A组 :(4 .49± 0 .6 0 )kPa(1kPa =0 .75mmHg) ;D组 :(1.39± 0 .75 )kPa ,差异有非常显著性 (P <0 .0 1)。再灌注 15min时 ,A组 :(4 .2 8± 0 .77)kPa ;D组 :(1.36± 0 .2 7)kPa ,差异有非常显著性 (P <0 .0 1)。缺血后发展压力恢复率在复灌后 5min内明显改善 ,A组 :(74.3± 8.4) % ,D组 :(98.6± 3.2 ) % ,差异有非常显著性 (P <0 .0 1)。结论 曲美它嗪对心肌缺血挛缩有明显的保护作用。
Objective To investigate the protective effect of trimetazidine (TMZ) on myocardial ischemic contracture. Methods Rats were divided into groups A, B, C and D4. A was given as a control group, and myocardial ischemia model was made by micro-perfusion (0 ~ 1ml / min). Trimetazidine (3mg / d × 7d) , TMZ of 1 × 10 -6 mol / L was added into the perfusate to observe the change of cardiac development pressure after ischemia. Results The oral trimetazidine, trimetazidine perfusion solution group compared with the control group, myocardial ischemic development pressure was significantly improved. At 30 minutes after ischemia, the difference was significant (P <0. 0) in group A (4.49 ± 0.60) kPa (1kPa = 0 .75mmHg) 1). At 15 min reperfusion, group A: (4.2 ± 0.77) kPa; group D: (1.36 ± 0.27) kPa, the difference was significant (P <0.01). The recovery rate of developmental pressure after ischemia was significantly improved within 5 min after reperfusion, with a significant difference (P <0.01) in group A (74.3 ± 8.4)% and group D (98.6 ± 3.2)%. Conclusion Trimetazidine has a significant protective effect on myocardial ischemic contracture.