普鲁卡因胺对犬冠心病心源性猝死实验模型的影响

Effects of procainamide on ventricular fibrillation in a canine model of sudden coronary death

用冠状动脉Harris二期结扎并部分再灌注法造成犬心肌梗塞,5—8天后,辅以冠状动脉内恒定微量直流电刺激法,研制成犬冠心病心源性猝死实验模型,并观察了普鲁卡因胺(PA)对该实验模型的影响,对该模型的可靠性、实用性及其临床相关性进行了探讨。结果表明,PA能有效地预防犬心肌梗塞后再缺血导致的室颤,该模型是一种有价值的冠心病猝死模型。

A canine model of sudden coronary death was established by intimal sur- face anodal direct current stimulation of the left circumflex coronary artery (LCX) on 5-8 days after the left anterior descending coronary artery (LAD) infarction. The LCX intimal injury and subsequent thrombus formation produced ECG ST segment chan- ges at 104±30 minutes (X±SD), followed by premature ventricular beats, ventricular tachycardia (VT), and ventricular fibrillation (VF) in all normal saline (NS) treated dogs (n=6), in procainamide (PA) treated dogs (n=6), ECG ST segment changes appeared at 110±40 minutes, followed by VT and VF in only one dog (P<0.05 vs NS). The results suggest that PA could prevent the onset of VT and VF resulting from ische- mia at a site distant to prior myocardial infarction in the dogs, and deserves further attention as an antifibrillatory agent for prevention of sudden coronary death in man, this canine model is a worthy and reliable model.