曲美他嗪对大鼠心力衰竭模型心肌能量代谢的干预

Intervention of Trimetazidine(TMZ) in The Myocardial Energy Metabolism of Heart Failure Model in Rats

目的探讨曲美他嗪对大鼠心力衰竭模型心肌能量代谢的干预作用。方法腹主动脉缩窄法制备SD大鼠心力衰竭模型,心脏超声测定室间隔(IVS)及左心室后壁(LVPW)厚度、左心室舒张末期内径(LVD)和收缩末期内径(LVS)、左心室射血分数(LVEF)和短轴缩短率(FS);电镜观察心肌线粒体结构变化;放射免疫法检测CA-ATP、游离脂肪酸(FFA)。结果曲美他嗪治疗组和模型组比较,IVST、LVPWT、LVESD、LVEDD明显缩小,LVEF、FS升高;线粒体结构明显改善;CA-ATP水平升高,FFA水平降低。结论曲美他嗪能改善大鼠心力衰竭模型心肌能量代谢,改善心功能。

Objective To observe the Intervention of trimetazidine （TMZ） in the myocardial energy metabolism of heart failure model in rats. Methods Partially banding abdominal aortic artery was used to achieve congestive heart failure rats model. Interventricular septum thickness（IVST） , left ventricular posterior wall thickness （LVPWT） , left ventricular end - diastolic diameter （LVEDD） , left ventricular end -systolic diameter（LVESD） ,left ventricular ejection fraction（LVEF） and shortening fraction（FS） were measured by echo- cardiogram. The myocardial mitochondrial structure was observed with electron microscopy. CA - ATP and free fatty acids （FFA） was meas- ured by radioimmunoassay method. Results As compared with model group,IVST, LVPWT,LVESD, LVEDD of TMZ treatment group de- creased obviously, LVEF and FS were markedly increased, the myocardial mitochondrial structure were remarkably improved, the level of CA - ATP was elevated, the level of FFA was decreased. Conclusion TMZ treatment can improve the abnormity of the myocardium en- ergy in the cardiac muscle cell of heart failure rats, and also obviously improve the cardiac contractility.