应用诱发心内膜反应评价抗心律失常药物对心肌的影响。

T. Furukawa, K. Taniguchi, J. Takeuchi
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引用次数: 0

摘要

“非对称双相刺激”技术可以对心脏进行起搏,并在电极-组织界面中和刺激后的极化,从而通过单个电极记录起搏和记录的整个心内膜反应。应用该系统研究了抗心律失常药物普鲁卡因胺和n -乙酰普鲁卡因胺对20只狗心肌的影响。在五步药物输注前和输注过程中,分别以120、150和200/min的速度记录双极和单极期间诱发的心内膜反应。普鲁卡因胺血药浓度范围为1.7 ~ 32.5 mg/l, n -乙酰普鲁卡因胺血药浓度范围为8.1 ~ 116.1 mg/l。普鲁卡因胺在低血浆浓度下显著延长去极化持续时间和复极化持续时间(一类抗心律失常药物性质)。n -乙酰普鲁卡因胺在低血药浓度下显著延长复极化持续时间,而在低血药浓度或治疗性血药浓度下去极化持续时间无显著变化(III类抗心律失常药物性质)。普鲁卡因酰胺和n -乙酰普鲁卡因酰胺对去极化持续时间的延长呈速率依赖性;速度越快,延长的时间就越长。简单准确地评价抗心律失常药物对心肌的作用,为今后的抗心律失常药物治疗提供了一种手段。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The use of evoked endocardial response for assessment of antiarrhythmic drug effects on myocardium.
The technique "asymmetric biphasic stimulation" which paces the heart and neutralizes the post-stimulus polarization at the electrode-tissue interface allows for the recording of the entire evoked endocardial response via a single electrode for both pacing and recording. Using this system the effects of antiarrhythmic drugs, procainamide and N-acetylprocainamide, on the myocardium were studied in 20 dogs. Before and during the five-step drug infusion, the evoked endocardial responses were recorded during bipolar and unipolar at the rates of 120, 150 and 200/min. The plasma concentration of the procainamide ranged from 1.7 to 32.5 mg/l and that of N-acetylprocainamide ranged from 8.1 to 116.1 mg/l. Procainamide significantly prolonged both the depolarization duration and the repolarization duration at a low plasma concentration (Class I antiarrhythmic drug property). N-acetylprocainamide significantly prolonged the repolarization duration at a low plasma concentration, while the depolarization duration was not significantly changed at a low or therapeutic plasma concentration (Class III antiarrhythmic drug property). The prolongation of the depolarization duration by procainamide and N-acetylprocainamide was rate-dependent; the faster the rate the greater the prolongation. This simple and accurate assessment of the antiarrhythmic drug effects on the myocardium may provide a future means for the pharmacologic antiarrhythmic therapy.
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