A canine model of ischemic ventricular tachyarrhythmias was established in open-chest dogs subjected to programmed electrical stimulation (PES) for 5￣8 days after acute myocardial infarction. The electrophysiologic effects of sophoridine (Sop) and procainamide (PA) were observed in this canine model. With routine methods of PES, ventricular tachycardia (VT) and ventricular fibrilation (VF) could be reproducibly initiated in this model. Both drugs distinctly lengthened the QTc interval ( P <0.01) and the effective refractory period (ERP) in normal and ischemic ventricular myocardium ( P <0.01), decreased the dispersion of ERP in ischemic myocardium and the dispersion of ERP in left ventricle (P <0.05), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardium remarkably ( P <0.01). Both drugs effectively prevented the PES-induced VT or VF and ischemia-induced VF ( P <0.05). The results indicated that this canine model is a good and reliable one, sophoridine and procainamide may be effective in preventing the onset of reentrant ventricular tachyarrhythmias after myocardial ischemic damage.
Objective To establish a canine model of electrophysiologic - electropharmacology as assessed by programmed electrical stimulation (PES),and to observe the electrophysiologic effects of Procainamide(PA) on normal and ischemic myocardium in case of ischemic ventricular tachyarrhythmia in this model. Methods A ishemic ventricular tachyarrhythmias canine model was established in open-chest dogs subjected to programmed electrical stimulation(PES)for 5-8 days after acute myocardial infarction. The electrophysiologic effects of procainamide were observed in this model. With routine methods of PES,ventricular tachycardia(VT) and ventricular fibrillation (VF) could be reproducibly initiated. Results Procainamide 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 the dispersion of ERP in left ventricle (P<0.01), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardium remarkably (P<0.01). Procainamide effectively prevented the PES-induced VT or VF (P<0.05) and ischemia-induced VF (P<0.05). Conclusion The results indicated that PES-induced VT/VF were highly reproducible and reliable, this canine model is a worthy and reliable one, procainamide may be effective in preventing the onset of VT and VF after myocardial ischemic damage, and deserves further attention as an antifibrillatory agent.
