阿托品在兔心房中的奎尼丁样活性。

Quinidine-like activity of atropine in rabbit atria.

作者信息

Holl J E

出版信息

Eur J Pharmacol. 1978 Feb 15;47(4):423-30. doi: 10.1016/0014-2999(78)90123-1.

Abstract

Direct effects of atropine and quinidine on contractile force, overdrive suppression, and effective refractory period was studied in rabbit atria. Left atrial contractile force at normal CaCl2 concentration (2.2 mM) and the contractile force response to elevated CaCl2 (5 mM) were unchanged over 30 min. Atropine exposure (1.7 X 10(-5) M) for 30 min significantly reduced contractile force at both normal and elevated CaCl2 levels. Quinidine exposure (6.2 X 10(-6) M) for 30 min produced similar but statistically insignificant changes. At 4 h, control contractile force at 2.2 mM CaCl2 decreased to the post-atropine level, but the response to 5 mM CaCl2 was unchanged. The asystolic interval of right atria following overdrive (for 2 min at 3 rates) was increased after 30 min by 4% for controls, 14% after atropine (1.7 X 10(-5) M) and 45% after quinidine. The effective refractory period of left atria (evaluated by paired pulse stimulation) was unchanged after 30 min for controls, but increased by 20% after atropine and 45% after quinidine.

摘要

研究了阿托品和奎尼丁对兔心房收缩力、超速抑制及有效不应期的直接作用。在正常氯化钙浓度（2.2 mM）下左心房收缩力以及对升高的氯化钙（5 mM）的收缩力反应在30分钟内未发生变化。暴露于阿托品（1.7×10⁻⁵ M）30分钟显著降低了正常和升高氯化钙水平下的收缩力。暴露于奎尼丁（6.2×10⁻⁶ M）30分钟产生了类似但无统计学意义的变化。在4小时时，2.2 mM氯化钙下的对照收缩力降至阿托品处理后的水平，但对5 mM氯化钙的反应未改变。右心房在超速驱动（以3种速率持续2分钟）后的停搏间期在30分钟后，对照组增加了4%，阿托品（1.7×10⁻⁵ M）处理后增加了14%，奎尼丁处理后增加了45%。左心房的有效不应期（通过配对脉冲刺激评估）在30分钟后，对照组未改变，但阿托品处理后增加了20%，奎尼丁处理后增加了45%。