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目的:观察脑心康2号对急性心肌缺血大鼠心肌损伤标志物及心功能的影响,并探讨其作用机制。方法:将8～10周龄Wistar大鼠60只随机分成6组:正常对照组、心肌缺血模型组(生理盐水)、阳性对照组(复方丹参滴丸8.4×10-2 g.kg-1)、脑心康2号高、中、低剂量(分别为含生药61,30.5,15.25 g.kg-1)组。除正常组外均给予相应药物ig,20 d后,分2次间隔24 h ip垂体后叶素(PIT)制备急性心肌缺血大鼠模型,于第2次注射30 min后ip 2%戊巴比妥钠40 mg.kg-1麻醉大鼠,测心电,分析心肌缺血阳性发生率,阳性对象行心脏彩超观察心功能左室射血分数(LVEF)、短轴缩短率(FS)、左室舒张末内径(LVEDD)、左室收缩末内径(LVESD)。3 h后采血,测定血清肌钙蛋白(cTnI)、肌红蛋白(MB)、肌酸激酶同工酶(CK-MB)含量。结果:脑心康2号高、中剂量组心肌损伤标志物的升高幅度明显低于模型组,心功能测得值明显优于模型组,其中高、中剂量组LVEF,FS,LVESD改善差异非常显著(P<0.05,P<0.01),低剂量组效果不明显。结论:脑心康2号对大鼠心肌具有保护作用,其机制可能与扩张心血管、增加血流量、改善血液循环、控制血小板的聚集、促进纤维蛋白的溶解、改善心肌酶的活性、减少心肌细胞损伤及增强心功能有关。
Objective: To observe the effects of Naoxinkang 2 on myocardial injury markers and cardiac function in acute myocardial ischemia rats and to explore its mechanism. Methods: Sixty Wistar rats aged 8 to 10 weeks were randomly divided into 6 groups: normal control group, model group with myocardial ischemia (saline), positive control group (8.4 × 10-2 g · kg-1 ), Naoxinkang 2 high, medium and low doses (containing crude drug 61,30.5,15.25 g.kg-1) group. In addition to the normal group were given the corresponding drug ig, 20 d later, divided into 2 times interval 24 h ip pituitrin (PIT) preparation of acute myocardial ischemia rat model, 30 min after the second injection of ip 2% pentobarbital The rats were anesthetized with 40 mg · kg-1 of sodium tetracycline, and the electrocardiogram was used to analyze the positive rate of myocardial ischemia. The positive rate of left ventricular ejection fraction (LVEF) Left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD). Blood samples were collected 3 h later, and the serum levels of cTnI, myoglobin and creatine kinase MB were measured. Results: The increase of myocardial injury markers in Naoxikang No.2 high and middle dose groups was significantly lower than that in model group, and the measured values of cardiac function were significantly better than those in model group. The differences of LVEF, FS and LVESD in high and middle dose groups were improved Very significant (P <0.05, P <0.01), the effect of low dose group was not obvious. CONCLUSION: Naoxinkang 2 has a protective effect on myocardium in rats. Its mechanism may be related to expanding cardiovascular, increasing blood flow, improving blood circulation, controlling platelet aggregation, promoting fibrinolysis, improving myocardial enzyme activity and reducing myocardial Cell damage and enhance cardiac function.