Objectives To observe the electrophysiologic effects of propafenone (Prop) on ischemic ventricular tachyarrhythmias. Methods A canine ischemic ventricular tachyarrhythmia model was established in open-chest dogs sub...Objectives To observe the electrophysiologic effects of propafenone (Prop) on ischemic ventricular tachyarrhythmias. Methods A canine ischemic ventricular tachyarrhythmia model was established in open-chest dogs subjected to programmed electrical stimulation (PES) on 5-8 days after acute myocardial infarction. The electrophysiologic effects of propafenone were observed in the model. Results Propafenone distinctly lengthened the QTc interval (P 〉 0.01) and effective refractory period (ERP) of normal and ischemic ventricular myocardium (NERP and IERP) respectively (P 〉 0.01), decreased the dispersion of ERP in ischemic myocardium and in left ventricle (P 〉 0.01), and increased the diastolic excitability threshold of normal and ischemic ventricular myoeardium remarkably (P 〉 0.01). Propafenone effectively prevented PES-induced ventricular tachycardia (VT) or ventricular fibrillation (VF) (P 〉 0.01) and ischemia-induced VT/VF (P 〉 0.05). Conclusions The results indicated that the canine model produced by our methods is a worthy and reliable one, propafenone may be effective in preventing the onset of VT / VF after myocardial ischemic damage in dogs, and deserve further attention as an antifibrillatory agent.展开更多
文摘Objectives To observe the electrophysiologic effects of propafenone (Prop) on ischemic ventricular tachyarrhythmias. Methods A canine ischemic ventricular tachyarrhythmia model was established in open-chest dogs subjected to programmed electrical stimulation (PES) on 5-8 days after acute myocardial infarction. The electrophysiologic effects of propafenone were observed in the model. Results Propafenone distinctly lengthened the QTc interval (P 〉 0.01) and effective refractory period (ERP) of normal and ischemic ventricular myocardium (NERP and IERP) respectively (P 〉 0.01), decreased the dispersion of ERP in ischemic myocardium and in left ventricle (P 〉 0.01), and increased the diastolic excitability threshold of normal and ischemic ventricular myoeardium remarkably (P 〉 0.01). Propafenone effectively prevented PES-induced ventricular tachycardia (VT) or ventricular fibrillation (VF) (P 〉 0.01) and ischemia-induced VT/VF (P 〉 0.05). Conclusions The results indicated that the canine model produced by our methods is a worthy and reliable one, propafenone may be effective in preventing the onset of VT / VF after myocardial ischemic damage in dogs, and deserve further attention as an antifibrillatory agent.