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目的:研究定心方(DXR)抗兔心肌缺血及再灌注损伤和抗心律失常作用。方法:兔冠状动脉双重结扎造成心肌梗塞,观察各组心律失常情况并检测血浆超氧化物歧化酶(SOD)、cAMP、去甲肾上腺素(NE)、多巴胺(DA)、5羟色胺(5HT),观察心肌超微结构。结果:DXR对兔心肌梗塞后心律失常有拮抗作用,其中DXR大剂量组与对照组比较有显著性差异(P<001);对缺血再灌注心律失常也有拮抗作用,DXR大、小剂量组与对照组比较均有显著性差异(P<001);对上述状态的心电图ST-T抬高有改善作用。实验表明,DXR能升高血清SOD浓度,而使cAMP、NE、DA、5HT浓度和全血粘度降低。结论:DXR能拮抗心肌缺血及再灌注损伤和心律失常,其机理可能通过清除氧自由基、调节细胞第二信使、抑制交感神经系统、改善局部循环,保护线粒体、抑制溶酶体活化使心肌细胞免受损伤而实现。
Objective: To study the effect of DXR on myocardial ischemia and reperfusion injury and antiarrhythmic effect in rabbits. METHODS: Myocardial infarction was induced by double coronary artery ligation in rabbits. Arrhythmia was observed in each group. Plasma superoxide dismutase (SOD), cAMP, norepinephrine (NE), dopamine (DA), and serotonin (5HT) were measured. Observe the ultrastructure of the myocardium. RESULTS: DXR had an antagonistic effect on arrhythmia after myocardial infarction in rabbits, among which DXR high-dose group had significant difference compared with control group (P < 001) and also had antagonistic effect on ischemia-reperfusion arrhythmia. DXR large and small dose group Compared with the control group, there was a significant difference (P<001); there was an improvement in ST-T elevation of the electrocardiogram in the above state. Experiments have shown that DXR can increase serum SOD concentration, while decreasing cAMP, NE, DA, 5HT concentration and whole blood viscosity. Conclusion: DXR can antagonize myocardial ischemia, reperfusion injury and arrhythmia. The mechanism may be through scavenging oxygen free radicals, regulating second cell messengers, inhibiting sympathetic nervous system, improving local circulation, protecting mitochondria, inhibiting lysosome activation and making myocardial The cells are protected from damage.