中文摘要：

目的：探讨丹参酮对兔心梗后恶性心律失常及钙调蛋白信号转导通路的影响。方法：将30只家兔随机均分为假手术组、模型组和丹参酮组,通过对冠状动脉左前降支进行结扎来建立急性心肌梗死模型,然后随机分为模型组和丹参酮组。观察并比较三组家兔恶性心律失常发生率、三层心肌（心内膜下层、心肌层和心外膜下层）中的动作电位时程、跨壁复极离散度、三层心肌细胞中的钙离子浓度、钙调蛋白和钙调蛋白激酶Ⅱ表达水平。结果：丹参酮组恶性心律失常发生率显著低于模型组（20.0%比70.0%,P〈0.01）;与假手术组比较,模型组和丹参酮组心内膜下层、心肌中层和心外膜下层的90%动作电位时程、跨壁复极离散度、钙离子浓度、钙调蛋白和钙调蛋白激酶Ⅱ表达水平显著升高（P均〈0.01）,且与模型组比较,丹参酮组三层心肌的跨壁复极离散度[（46.2±10.9）ms比（35.5±8.8）ms],90%动作电位时程[心外膜下层,（231.5±17.4）ms比（211.0±16.3）ms]、钙离子浓度[心外膜下层,（132.0±12.3）mmol/L比（102.3±10.3）mmol/L]、钙调蛋白[心外膜下层,（0.724±0.014）比（0.563±0.014）]和钙调蛋白激酶Ⅱ[心外膜下层,（0.759±0.019）比（0.589±0.017）]表达水平均显著降低（P〈0.05~〈0.01）。结论：丹参酮具有抗心肌梗死后恶性心律失常的作用,其作用机制可能为调节钙调蛋白和钙调蛋白激酶Ⅱ信号转导通路。

英文摘要：

Objective.. Abstract： Objective： To explore influence of tanshinone on rabbit malignant arrhythmias and calmodulin signal transduction pathway after myocardial infarction. Methods： A total of 30 rabbits were randomly and equally divided into sham operation group （sham group）, model group and tanshinone group. Acute myocardial infarction model was established through ligating left anterior descending branch of coronary. After modeling, the rabbits were randomly and equally divided into model group and tanshinone group. Incidence rate of malignant ar- rhythmias, action potential duration （APD） of three myocardial layers （namely endocardium layer, myocardium layer and epicardium layer）, transmural dispersion of repolarization, Ca2＋ concentration, expression levels of calm- odulin and calmodulin kinase I] in three myocardial layers were observed and compared＇ among three groups. Re- suits, Incidence rate of malignant arrhythmias in tanshinone group was significantly lower than that of model group （20.0% vs. 70, 0%, P〈0.01） ; compared with sham group, there were significant rise in transmural dispersion of repolarization, 90% APD, Caz＋ concentration, expression levels of calmodulin and calmodulin kinase 1] of three layers in model group and tanshinone group （P〈0.01 all）; compared with model group, there were significant re- ductions in transmural dispersion of repolarization [ （46.2±10. 9） ms vs. （35.5±8. 8） ms], 90% APD [epicardium layer, （231.5±17.4） ms vs. （211.0±16.3） ms], Ca2＋ concentration [epicardium layer, （132.0±12.3） mmol/L vs. （102.3±10.3） mmol/L], expression levels of calmodulin [-epicardium layer, （0. 724±0. 014） vs. （0. 563±O. 014）] and calmodulin kinase 11 [epicardium layer, （0. 759±0. 019） vs. （0. 589±0. 017）] in tanshinone group, （P〈0.05～ 〈0.01）. Conclusion： Tanshinone possesses anti-malignant arrhythmias effect after myocardial infarc- tion. Its mechanism may be regulating calmodulin and calmodulin kin