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人体心室的强度-间期关系:普鲁卡因胺的作用

Strength-interval relation in the human ventricle: effect of procainamide.

作者信息

Camardo J S, Greenspan A M, Horowitz L N, Spielman S R, Josephson M E

出版信息

Am J Cardiol. 1980 Apr;45(4):856-60. doi: 10.1016/0002-9149(80)90132-0.

DOI:10.1016/0002-9149(80)90132-0
PMID:7361675
Abstract

The effects of procainamide on strength-interval relations were evaluated in 18 patients. At plasma concentrations of 4.3 to 13.6 micrograms/ml procainamide had minimal effects on threshold current in late diastole, but in early diastole it shifted the strength-interval curve to the right. The basic strength-interval relation (that is, decreasing refractory period as current is increased) was not altered. The control refractory period decreased by a mean of 44 ms as the current was increased from threshold to 10 mA, whereas a mean decrease of 42 ms was observed after procainamide. However, the steep portion of the strength-interval curve(absolute refractory period) was shifted to longer coupling intervals by a mean value of 24 ms. These findings suggest that procainamide may primarily affect active membrane properties, but exert little net effect on passive membrane properties late in diastole.

摘要

在18名患者中评估了普鲁卡因胺对强度-间期关系的影响。血浆浓度为4.3至13.6微克/毫升时,普鲁卡因胺对舒张晚期的阈电流影响极小,但在舒张早期,它使强度-间期曲线右移。基本的强度-间期关系(即随着电流增加,不应期缩短)未改变。当电流从阈值增加到10毫安时,对照的不应期平均缩短44毫秒,而使用普鲁卡因胺后平均缩短42毫秒。然而,强度-间期曲线的陡峭部分(绝对不应期)平均右移24毫秒至更长的耦联间期。这些发现表明,普鲁卡因胺可能主要影响细胞膜的主动特性,但在舒张晚期对细胞膜的被动特性几乎没有净效应。

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引用本文的文献

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Induction of ventricular arrhythmias by programmed ventricular stimulation: a prospective study on the effects of stimulation current on arrhythmia induction.程控心室刺激诱发室性心律失常:刺激电流对心律失常诱发影响的前瞻性研究
Br Heart J. 1987 Nov;58(5):489-94. doi: 10.1136/hrt.58.5.489.
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Can the technicalities of electrophysiological testing for ventricular tachycardia be simplified?室性心动过速的电生理检查技术能否简化?
Br Heart J. 1987 Nov;58(5):437-40. doi: 10.1136/hrt.58.5.437.
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Effect of mexiletine, amiodarone and disopyramide on the excitability and refractoriness of canine cardiac fibers: possible relation to antiarrhythmic drug action and classification.
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