Undrovinas A I, January C, Iuriavichus I, Riddle J, Zablotskaĭte D
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR. 1989;12(1):6-11.
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.
研究了钙电流激动剂BAY K 8644对豚鼠乳头肌（PM）和绵羊浦肯野纤维（PF）跨膜电位的影响。记录了动作电位（AP）和收缩（C）。加入BAY K 8644（0.5 - 5微摩尔）后，PM和PF的C均增加（两到四倍）。PM的AP时程略有增加（20%），而即使在低剂量BAY K 8644（0.5微摩尔）时，PF的AP时程也随时间逐渐增加。在第5分钟时，出现了早期后去极化（EAD）。给药10分钟后，PF在高平台期变得不可兴奋。河豚毒素（TTX）和乙吗噻嗪（1微摩尔）可恢复AP。因此，BAY K 8644使PF中的离子电流平衡朝着内向钙电流增加的方向变化，导致平台期出现额外的稳态电位。后者可能诱发EAD并在功能上不可兴奋的PF周围形成折返。文中讨论了缺血诱导的心律失常机制与该模型的相似性。
