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普鲁卡因酰胺在低于治疗剂量至治疗剂量时对人体房室传导系统的电生理效应。

Electrophysiologic effects of procainamide in subtherapeutic to therapeutic doses on human atrioventricular conduction system.

作者信息

Ogunkelu J B, Damato A N, Akhtar M, Reddy C P, Caracta A R, Lau S H

出版信息

Am J Cardiol. 1976 Apr;37(5):724-31. doi: 10.1016/0002-9149(76)90366-0.

DOI:10.1016/0002-9149(76)90366-0
PMID:773160
Abstract

The effects of single intravenous infusions of 50 to 400 mg of procainamide on the functional properties of the atrioventricular (A-V) conduction system were studied in 36 patients and correlated with plasma concentrations. A 50 mg dose of procainamide resulted in a plasma concentration of less than 1.0 mug/ml and produced no electrophysiologic changes. Doses of 100, 200, 300 and 400 mg resulted in progresively increasing plasma concentrations (1.2, 1.8, 3.5 and 4.2 mug/ml, respectively). The effects of procainamide on the sinus rate were variable and not dose-related. The effects of doses of up to 300 mg on A-V nodal conduction were variable and not dose-related. Only in a dose of 400 mg did procainamide prolong A-V nodal conduction in six of seven patients. Whereas 100 mg had no effect on His-Purkinje system conduction, doses of 200, 300 and 400 mg prolonged His-Purkinje system conduction time by 6, 8 and 9 msec, respectively. Dose-related increases in atrial refractoriness started with a dose of 200 mg and became statistically significant with doses of 300 and 400 mg. The effects of procainamide on A-V nodal functional refractoriness were variable and not dose-related, but in doses of 100 to 400 mg, procainamide produced significant and progressively dose-related increases in His-Purkinje system refractoriness. Suppression of some types of ventricular arrhythmia by small doses of this drug may be explained by changes in refractoriness of the His-Purkinje system produced by doses of procainamide as small as 100 mg.

摘要

在36例患者中研究了单次静脉输注50至400毫克普鲁卡因胺对房室(A-V)传导系统功能特性的影响,并与血浆浓度进行了相关性分析。50毫克剂量的普鲁卡因胺导致血浆浓度低于1.0微克/毫升,未产生电生理变化。100、200、300和400毫克剂量导致血浆浓度逐渐升高(分别为1.2、1.8、3.5和4.2微克/毫升)。普鲁卡因胺对窦性心率的影响是可变的,且与剂量无关。高达300毫克剂量对A-V结传导的影响是可变的,且与剂量无关。仅在400毫克剂量时,普鲁卡因胺使7例患者中的6例A-V结传导延长。100毫克对希氏-浦肯野系统传导无影响,而200、300和400毫克剂量分别使希氏-浦肯野系统传导时间延长6、8和9毫秒。心房不应期与剂量相关的增加始于200毫克剂量,在300和400毫克剂量时具有统计学意义。普鲁卡因胺对A-V结功能不应期的影响是可变的,且与剂量无关,但在100至400毫克剂量时,普鲁卡因胺使希氏-浦肯野系统不应期显著增加且与剂量相关。小剂量该药物对某些类型室性心律失常的抑制作用可能是由于小至100毫克剂量的普鲁卡因胺引起的希氏-浦肯野系统不应期变化所致。

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Electrophysiologic effects of procainamide in subtherapeutic to therapeutic doses on human atrioventricular conduction system.普鲁卡因酰胺在低于治疗剂量至治疗剂量时对人体房室传导系统的电生理效应。
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Intracardiac electrophysiological effects of lorcainide in man.
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