Kupersmith J, Hoff P
J Am Coll Cardiol. 1985 Jul;6(1):152-62. doi: 10.1016/s0735-1097(85)80267-9.
Abnormal delay of repolarization leading to prolonged reduction of membrane potential could lead to arrhythmias. Transmission of this type of abnormality from an "abnormal" to a "normal" segment of Purkinje fiber was studied as follows: In a double compartment bath one segment was superfused with unmodified Tyrode's solution and the other with solutions known to induce abnormal prolongation of action potential duration (manifest by prolonged step-like delays in repolarization, or "secondary plateaus" and "early afterdepolarization," that is, activations arising as a consequence of the prolonged depolarized membrane potential). Transmission of abnormalities varied. Complete transmission of secondary plateaus and early afterdepolarizations led to action potentials configurationally similar throughout the fiber. Selective transmission of early afterdepolarization led to the occurrence of new premature action potentials in the normal segment. Cycle length prolongation favored both the occurrence and the transmission of abnormalities. After addition of lidocaine or high potassium ion solutions to the normal segment, shortening of action potential duration occurred and was transmitted from normal to abnormal segment. In this way, reversal of abnormality throughout the fiber occurred via an intervention applied selectively to the normal segment. Observations in this study may be relevant to arrhythmias and their treatment.
复极化异常延迟导致膜电位持续降低，可能引发心律失常。以下是对这种异常从浦肯野纤维的“异常”节段向“正常”节段传导的研究：在双隔室浴槽中，一个节段用未改良的台氏液灌流，另一个节段用已知能诱导动作电位时程异常延长的溶液灌流（表现为复极化过程中出现延长的阶梯状延迟，或“继发性平台期”和“早期后去极化”，即因膜电位持续去极化而产生的激活）。异常的传导情况各异。继发性平台期和早期后去极化的完全传导导致整个纤维的动作电位在形态上相似。早期后去极化的选择性传导导致正常节段出现新的过早动作电位。心动周期延长有利于异常的发生和传导。向正常节段添加利多卡因或高钾离子溶液后，动作电位时程缩短，并从正常节段传导至异常节段。通过选择性地作用于正常节段，可使整个纤维的异常情况发生逆转。本研究中的观察结果可能与心律失常及其治疗有关。
