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利多氟嗪对电压钳制的蛙心房肌纤维膜电流和收缩的影响。

Effect of lidoflazine on membrane currents and contraction in voltage-clamped frog atrial fibers.

作者信息

Einwächter H M, Kern R, Herb J

出版信息

Eur J Pharmacol. 1979 May 1;55(3):225-32. doi: 10.1016/0014-2999(79)90188-2.

Abstract

The effect of lidoflazine on action potential, membrane currents and contraction of frog atrial fibers was tested using the double sucrose voltage clamp technique. Lidoflazine was found to decrease the sodium conductivity of the heart cell membrane, probably by blocking the sodium channels. The availability of the sodium system at resting potential was slightly enlarged by lidoflazine and the recovery from inactivation was prolonged in most of the preparations tested. A small decrease of the slow inward current and a reduction of phasic and tonic tension was observed. The outward current at higher depolarizations was increased by lidoflazine resulting in a shortened action potential duration. The data suggest that lidoflazine's antifibrillatory properties are less pronounced than those of classical antiarrhythmic agents; but the slight antifibrillatory and negative inotropic effect might be helpful in the treatment of angina pectoris.

摘要

使用双蔗糖电压钳技术测试了利多氟嗪对蛙心房纤维动作电位、膜电流和收缩的影响。发现利多氟嗪可能通过阻断钠通道来降低心肌细胞膜的钠电导率。在大多数测试制剂中,利多氟嗪使静息电位时钠系统的可用性略有增加,并延长了失活后的恢复时间。观察到缓慢内向电流略有降低,以及相性和强直性张力降低。利多氟嗪使较高去极化时的外向电流增加,导致动作电位时程缩短。数据表明,利多氟嗪的抗纤颤特性不如经典抗心律失常药物明显;但其轻微的抗纤颤和负性肌力作用可能有助于治疗心绞痛。

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