长期吸食二乙酰吗啡可致心源性猝死，心律失常是心源性猝死的主要原因。阿片受体和CaMKⅡ信号通路在心律失常中发挥重要作用，但阿片受体是否调节CaMKⅡ信号通路在二乙酰吗啡致心律失常的作用机制尚未见报道；基于前期研究及文献，阿片受体可调节Ca2+/CaMKⅡ信号通路与二乙酰吗吗啡致心律失常的发生机制相关。因此，拟采用心律失常动物模型和细胞培养模型，对在体心肌、离体心肌细胞和心肌单细胞从组织、细胞分子等多个水平，分析二乙酰吗啡致心律失常与何种阿片受体相关、是否诱导[Ca2+]i大量内流而激活CaMKⅡ信号通路使SR内储Ca2+释放、筛选阿片受体调节Ca2+/CaMKⅡ信号传导中的关键分子、是否改变细胞和线粒体膜电位致钙离子大量释放；旨在明确阿片受体/Ca2+/CaMKⅡ信号通路在二乙酰吗啡致心律失常中的重要作用和阿片受体、CaMKⅡ是否可作为抗心律失常的靶点，为临床防治及药物靶点研究提供依据。

Long-term consumption of diacetyl morphine can cause sudden cardiac death, arrhythmia is the main cause of sudden cardiac death.Opioid receptors and CaMKII signaling pathway play an important role in cardiac arrhythmia. However, the mechanism by which opioid receptors regulate CaMKII signaling pathway in diacetylmorphine induced arrhythmias has not been reported.Based on the previous studies and literature, opioid receptors regulating Ca2 + / CaMKII signaling pathway is related to the mechanism of arrhythmia induced by diacetyl morphine.Therefore, the arrhythmia animal model and cell culture model are to be used to analyze the in vivo myocardium, isolated cardiomyocytes and single cells of myocardium from tissues, cell molecules and other levels.To analyze whether diacetylmorphine-induced arrhythmia is associated with which opioid receptor, and whether Ca2 + / CaMKII signal transduction leads to Ca2 + / CaMKII signal transduction, and hether to change the cellular and mitochondrial membrane potential caused by a large number of release of calcium ions. And we will screen of key molecules of opioid receptors regulates Ca2 + / CaMKII signaling.To clarify whether opioid receptor / Ca2 + / CaMKII signaling pathway plays an important role in diacetylmorphine induced arrhythmia and whether opioid receptor and CaMKII can be used as anti-arrhythmic targets, so we can provide evidences for clinical prevention and drug targets.