Childers R W
Pacing Clin Electrophysiol. 1984 Nov;7(6 Pt 2):1115-20. doi: 10.1111/j.1540-8159.1984.tb05670.x.
The major advance in our understanding of supernormality is the following hypothesis. Focal accumulations of extruded potassium ion in unstirred-clefts (invaginated extensions of the extracellular space in Purkinje fibers) cause threshold to fall by virtue of the early effects of hyperkalemia: lowering of threshold and acceleration of conduction. These effects rapidly dissipate in diastole as ionic equilibration takes place; threshold rises and assumes its late diastolic value. It is not known if this mechanism is applicable to the supernormality of specialized atrial fibers. Comparing the strength interval curves of supernormality and triggered automaticity the fall in threshold during the upstroke of the late after-depolarisation occurs later than the supernormal phase and is followed by a threshold rise (during the downstroke of the after-potential). Supernormality does not correspondingly show this biphasic change in the strength interval curve.
我们对超常期理解的主要进展如下假设。在未搅动裂隙(浦肯野纤维中细胞外空间的内陷延伸)中挤压出的钾离子的局部聚集,由于高钾血症的早期效应导致阈值下降:阈值降低和传导加速。随着离子平衡的发生,这些效应在舒张期迅速消散;阈值上升并恢复其舒张晚期值。尚不清楚这种机制是否适用于特殊心房纤维的超常期。比较超常期和触发自动节律的强度-间期曲线,晚后去极化上升支期间的阈值下降发生在超常期之后,随后阈值上升(在后电位的下降支期间)。超常期在强度-间期曲线中并未相应地显示出这种双相变化。