【摘要】 【目的】建立小鼠轻度病毒性心肌炎及其猝死模型。【方法】以CoxsackieB3 病毒感染Balb/c小鼠造成小鼠轻度病毒性心肌炎 ,以低剂量乌头碱为诱因 ,诱发心肌炎小鼠产生室性心律失常致死。【结果】感染小鼠出现轻度心肌炎改变。随心率离散度 (HRD)的下降 ,从 2 8～ 36min-1,17～ 2 5min-1至 8～ 13min-1递减 ,心肌炎小鼠经乌头碱诱发心律失常致死的比率增高 ,室性心律失常的出现率依次递增为 33 % ,6 4% ,89%。【结论】成功地建立了轻度病毒性心肌炎及其猝死模型。心肌电生理不稳定与一过性危险因素的相互作用可能为轻度病毒性心肌炎猝死的机制之一。更多还原

【Abstract】 Objective To establish the model of sudden death in mice with mild viral myocarditis . Methods Mild viral myocarditis model was produced in Balb/c mice by Coxsackie virus B 3. Fatal ventricular arrhythmias in mice with myocarditis were induced by giving mice a small amount of aconitine. Results Mild viral myocarditis model was successfully produced in mice.The rate of ventricular arrhythmias caused by aconitine increased (from 33%,64% to 89%) with the decrease (HRD from 28～36 min -1 ,17～25 min -1 to 8～13 min -1 ) of heart rate dispersion in mice with myocarditis. Conclusion Mild viral myocarditis model is successfully established in mice.The interplay of unstability of myocardial electrophysiology and transient risk factor may be responsible for sudden death in mice with mild viral myocarditis.更多还原