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目的探讨大鼠心肌梗死后交感神经重构现象以及美托洛尔对重构的抑制作用。方法心肌梗死模型成功后的48只大鼠随机分为心肌梗死组(A组)和美托洛尔治疗组[B组,10mg/(kg.d)]。各组分别在3个不同的时间点(3d、7d、30d)进行观测。各时间点配以相同只数的大鼠,只穿线不结扎作为对照组。测定大鼠心电图,并计算QT离散度(QTd)。连续记录大鼠心电图,并对心律失常进行评分。用免疫组化的方法检测各组大鼠心肌梗死周边区交感神经密度。结果A组7d、30d时心肌梗死周围区交感神经密度与对照组比有明显增加(P<0.05)。B组在第30天时,梗死周边区交感神经支配密度要明显低于同时间点的A组(P<0.05)。美托洛尔治疗后各时间点QTd和心律失常评分均比相应A组显著降低(P<0.05)。结论美托洛尔能抑制心肌梗死后交感神经的重构,降低QTd和心律失常,第30天时,美托洛尔对降低心律失常的作用部分是通过抑制交感神经重构介导的。
Objective To investigate the sympathetic nerve remodeling after myocardial infarction in rats and the effect of metoprolol on the remodeling. Methods Forty-eight MI rats were randomly divided into AMI (group A) and metoprolol (group B, 10 mg / (kg · d)]. Each group was observed at three different time points (3d, 7d, 30d). At each time point with the same number of rats, only the thread is not ligated as a control group. Rat electrocardiogram was measured and QT dispersion was calculated. Rat electrocardiogram was recorded continuously and the arrhythmia was scored. Immunohistochemistry was used to detect the density of sympathetic nerves around the myocardial infarction in each group. Results In group A, the density of sympathetic nerves around myocardial infarction was significantly increased at 7d and 30d compared with the control group (P <0.05). In group B, on the 30th day, the density of sympathetic innervation in infarct border area was significantly lower than that in group A at the same time point (P <0.05). Metoprolol treatment at each time point QTd and arrhythmia scores were significantly lower than the corresponding A group (P <0.05). Conclusion Metoprolol can inhibit sympathetic remodeling after myocardial infarction and reduce QTd and arrhythmia. At day 30, the effect of metoprolol on reducing arrhythmia is partly mediated by inhibition of sympathetic remodeling.