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目的:观察诺迪康对心肌缺血-再灌注损伤大鼠血流动力学的影响。方法:选取心电图正常SD大鼠,缺血前30 min经十二指肠注射给药,结扎大鼠冠状动脉左前降支30 min后,再灌注60 min,建立心肌缺血-再灌注损伤模型。观察在急性缺血和再灌注状态下血流动力学的心率(hart rate,HR)、左心室收缩压(LVSP)、左心室内压最大上升速率(+dp/dtmax)、左心室内压最大下降速率(-dp/dtmax)、左心室舒张压(LVDP)和左心室舒张末期压力(LVDEP)指标的变化。再灌注结束后,TTC法测量心肌梗死面积。结果:诺迪康能改善大鼠心肌缺血-再灌注后的血流动力学变化,HR、LVSP、+dp/dtmax和-dp/dtmax均较模型组升显著高(P<0.05),LVDP、LVDEP显著降低(P<0.05);同时可减少心肌梗死面积。结论:诺迪康能改善急性心肌缺血-再灌注损伤大鼠的血流动力学改变,对心肌缺血-再灌注损伤有保护作用。
Objective: To observe the effect of Nuodikang on the hemodynamics of myocardial ischemia-reperfusion injury in rats. Methods: SD rats with normal electrocardiogram (ECG) were selected and administered intraduodenally 30 minutes before ischemia. Ligation of left anterior descending coronary artery of rats for 30 min followed by 60 min reperfusion was performed to establish a myocardial ischemia-reperfusion injury model. The hemodynamics such as hart rate (HR), left ventricular systolic pressure (LVSP), maximal rate of increase of left ventricular pressure (+ dp / dtmax) and left ventricular pressure were observed during acute ischemia and reperfusion. (-dp / dtmax), left ventricular diastolic pressure (LVDP) and left ventricular end-diastolic pressure (LVDEP). After reperfusion, myocardial infarction size was measured by TTC method. RESULTS: Nuodixil could ameliorate the changes of hemodynamics after myocardial ischemia / reperfusion in rats. The levels of HR, LVSP, + dp / dtmax and -dp / dtmax were all significantly higher than those in model group (P < , LVDEP was significantly lower (P <0.05); at the same time can reduce the area of myocardial infarction. CONCLUSION: Nordicon can improve the hemodynamic changes of acute myocardial ischemia-reperfusion injury in rats, and has a protective effect on myocardial ischemia-reperfusion injury.