[Asymmetrical changes in electrical activity of Purkinje fibers and muscle cells after administration of BAY K 8644. A new model of cardiac arrhythmia].

A I Undrovinas, C January, I Iuriavichus, J Riddle, D Zablotskaĭte
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引用次数: 0

Abstract

The effects of calcium current agonist BAY K 8644 on transmembrane potential of guinea pig papillary muscle (PM) and sheep Purkinje fibers (PF) were studied. The action potentials (AP) and contractions (C) were recorded. C both of PM and PF increased (two-four times) in response to BAY K 8644 (0.5-5 microM) addition. The AP duration of PM increased slightly (20%) while PF AP duration increased progressively with the time even at low BAY K 8644 dose (0.5 microM). At 5th min, early afterdepolarizations (EAD) occurred. After 10 min drug application PF became inexcitable at high plateau level. TTX and ethmozin (1 microM) restored AP. Thus, changes in ionic currents balance in PF towards the increase in inward calcium current by BAY K 8644 resulted in additional steady state potential at plateau level. The latter might induce EAD and re-entry around functionally inexcitable PF. The similarity of mechanisms of arrhythmias induced by ischemia with the presented model is discussed.

服用BAY K 8644后浦肯野纤维和肌肉细胞电活动的不对称变化。心律失常的一种新模型。
研究了钙电流激动剂BAY k8644对豚鼠乳头肌(PM)和绵羊浦肯野纤维(PF)跨膜电位的影响。记录动作电位(AP)和收缩电位(C)。添加BAY k8644 (0.5 ~ 5 μ m)后,PM和PF的C均增加2 ~ 4倍。即使在低剂量(0.5 μ m)下,PM的AP持续时间也略有增加(20%),而PF的AP持续时间随着时间的增加而逐渐增加。第5分钟发生早期后去极化(EAD)。用药10分钟后,PF在高平台水平变得不可兴奋。TTX和ethmozin(1微米)恢复了AP。因此,BAY K 8644对PF内钙电流增加的离子电流平衡的改变导致了平台水平的额外稳态电位。后者可能导致EAD和功能性不可兴奋性PF周围的再进入。讨论了缺血引起心律失常的机制与所提出的模型的相似性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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