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五种β-肾上腺素能受体阻滞剂对离体血液灌注犬心房窦房传导时间的比较研究。

Comparative study of five beta-adrenoceptor blocking agents on sinoatrial conduction time in isolated blood-perfused canine atria.

作者信息

Shimotori M, Kobayashi M, Chiba S

出版信息

Arch Int Pharmacodyn Ther. 1985 Apr;274(2):240-52.

PMID:2862847
Abstract

We studied the effects of five beta-adrenoceptor blocking agents (propranolol, atenolol, sotalol, oxprenolol and carteolol) on sinus cycle length (SCL), sinoatrial conduction time (SACT) measured with a constant atrial pacing technique, and atrial developed tension (DT), using isolated blood-perfused canine atria. Except for carteolol, all tested beta-blockers were infused into the sinus node artery at a rate of 1-4 micrograms/min, and carteolol was given continuously at a rate of 0.1-0.4 micrograms/min. Atenolol and sotalol as well as propranolol prolonged SCL and SACT and reduced DT dose-dependently, although propranolol had more potent negative chrono-, dromo- and inotropisms than atenolol and sotalol. Oxprenolol did not change SCL significantly, but lengthened SACT at higher doses and decreased DT in a dose-related manner. Carteolol did not cause any significant changes in the three parameters. The relative potencies on deceleration of SA conduction on the basis of administration of doses which seems to be equipotent as to beta-blocking effect are as follows: propranolol greater than atenolol = sotalol greater than oxprenolol = carteolol. These results suggest that the membrane stabilizing action of beta-blockers may lengthen SACT but that the intrinsic sympathomimetic action of beta-blockers may resist such a prolongation of SACT.

摘要

我们使用离体血液灌注犬心房,研究了五种β-肾上腺素受体阻滞剂(普萘洛尔、阿替洛尔、索他洛尔、氧烯洛尔和卡替洛尔)对窦性周期长度(SCL)、采用恒定心房起搏技术测量的窦房传导时间(SACT)以及心房舒张期张力(DT)的影响。除卡替洛尔外,所有受试β受体阻滞剂均以1 - 4微克/分钟的速率注入窦房结动脉,卡替洛尔则以0.1 - 0.4微克/分钟的速率持续给药。阿替洛尔、索他洛尔以及普萘洛尔均剂量依赖性地延长SCL和SACT并降低DT,尽管普萘洛尔的负性变时、变传导和变力作用比阿替洛尔和索他洛尔更强。氧烯洛尔对SCL无显著影响,但在较高剂量时延长SACT并以剂量相关方式降低DT。卡替洛尔对这三个参数均未引起任何显著变化。基于似乎具有等效β受体阻滞作用的给药剂量,β受体阻滞剂对窦房传导减慢的相对效力如下:普萘洛尔>阿替洛尔 = 索他洛尔>氧烯洛尔 = 卡替洛尔。这些结果表明,β受体阻滞剂的膜稳定作用可能会延长SACT,但β受体阻滞剂的内在拟交感神经作用可能会抵抗SACT的这种延长。

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