摘要
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.
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.
