Kingma J H, de Graeff P A, van Gilst W H, van Binsbergen E, de Langen C D, Wesseling H
Postgrad Med J. 1986;62 Suppl 1:159-63.
The effect of captopril on inducible sustained ventricular tachycardia (VT) one week after myocardial infarction was studied in 6 Yorkshire swine. In 24 pigs, controlled myocardial infarction (MI) was produced by reversible occlusion of the left anterior descending artery during 60 minutes using an inflatable balloon catheter. Four animals died during this procedure and another 4 during the first week. After 7 days, programmed electrical stimulation (PES) was performed in the surviving animals. Seven animals showed inducible VT, which could not be terminated in one. Subsequently, intravenous captopril (0.6-1.2 mg/kg) was administered as a rapid bolus injection. PES was repeated after 5 minutes and VT was no longer inducible in all 6 pigs (P less than 0.05). Right ventricular refractoriness decreased from 253 to 228 ms (n.s.). Blood pressure and heart rate were not significantly changed. We conclude that captopril can protect the heart against PES-induced VT late after MI. It is suggested that inhibition of angiotensin II and subsequent inhibition of noradrenaline may be responsible for this effect.
在6只约克郡猪身上研究了卡托普利对心肌梗死后1周诱发的持续性室性心动过速（VT）的影响。在24只猪中，使用可充气气球导管在60分钟内可逆性闭塞左前降支动脉，造成可控性心肌梗死（MI）。在此过程中有4只动物死亡，另有4只在第一周内死亡。7天后，对存活的动物进行程序电刺激（PES）。7只动物显示可诱发室性心动过速，其中1只不能终止。随后，静脉快速推注卡托普利（0.6 - 1.2 mg/kg）。5分钟后重复进行PES，所有6只猪均不再能诱发室性心动过速（P < 0.05）。右心室不应期从253毫秒降至228毫秒（无统计学意义）。血压和心率无明显变化。我们得出结论，卡托普利可保护心脏免受心肌梗死后晚期程序电刺激诱发的室性心动过速的影响。提示血管紧张素II的抑制以及随后去甲肾上腺素的抑制可能是此效应的原因。
