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普鲁卡因胺对人体希氏-浦肯野系统内折返的消除与改变

Abolition and modification of reentry within the His-Purkinje system by procainamide in man.

作者信息

Reddy C P, Lynch M

出版信息

Circulation. 1978 Dec;58(6):1010-22. doi: 10.1161/01.cir.58.6.1010.

Abstract

The effects of intravenous procainamide infusion of 10--14 mg/kg body weight (i.e., 750 mg) of procainamide (PA) on reentry within the His-Purkinje system (HPS) were studied in 13 patients using His bundle electrograms and ventricular extrastimulus method. PA abolished reentry in eight patients (group 1) and decreased the width of reentry zone in the remaining five (group 2). At comparable S1S2 intervals, the S2H2 intervals after PA were longer than control in all patients. In group 1 patients, after PA, reentry did not occur even at S2H2 intervals that were significantly longer than control critical S2H2 intervals. In two of eight patients in group 1, PA abolished reentry by converting unidirectional block into bidirectional block in the antegrade limb (right bundle) of the reentry circuit. In the remaining six patients reentry was abolished because of consistent retrograde block of S2 impulse at some point between the site of stimulation and the His bundle recording site. In group 2, reentry was initiated after PA at approximately the same S1S2 intervals as in control, but required significantly longer S2H2 intervals; in these patients the zone of reentry was shortened due to increase in effective refractory period of the ventricular muscle. PA significantly increased the functional refractory period of HPS and the effective refractory period of ventricular muscle. The results of this study differ from the previously reported effects of lower concentrations of PA which facilitated reentry within the same circuit. We conclude that the effects of PA on reentry are dose-related and can both facilitate and suppress reentry, depending on critical changes in conduction and refractoriness of the HPS.

摘要

采用希氏束电图和心室期外刺激法,对13例患者静脉输注10 - 14mg/kg体重(即750mg)普鲁卡因胺(PA)对希氏 - 浦肯野系统(HPS)内折返的影响进行了研究。PA使8例患者(第1组)的折返消失,其余5例(第2组)的折返区宽度减小。在可比的S1S2间期,所有患者PA后的S2H2间期均长于对照。在第1组患者中,PA后,即使S2H2间期明显长于对照临界S2H2间期,折返也未发生。在第1组的8例患者中有2例,PA通过将折返环前向支(右束支)的单向阻滞转变为双向阻滞而消除了折返。在其余6例患者中,折返消失是因为S2冲动在刺激部位与希氏束记录部位之间的某个点持续出现逆行阻滞。在第2组中,PA后在与对照大致相同的S1S2间期引发折返,但需要明显更长的S2H2间期;在这些患者中,由于心室肌有效不应期增加,折返区缩短。PA显著增加了HPS的功能不应期和心室肌的有效不应期。本研究结果与先前报道的较低浓度PA促进同一环路内折返的作用不同。我们得出结论,PA对折返的作用与剂量相关,并且根据HPS传导和不应期的关键变化,既可以促进也可以抑制折返。

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