Rationale: The development of a refractory period for Ca²⁺ spark initiation after Ca²⁺ release in cardiac myocytes should inhibit further Ca²⁺ release during the action potential plateau. However, Ca²⁺ release sites that did not initially activate or which have prematurely recovered from refractoriness might release Ca²⁺ later during the action potential and alter the cell-wide Ca²⁺ transient.

Objective: To investigate the possibility of late Ca²⁺ spark (LCS) activity in intact isolated cardiac myocytes using fast confocal line scanning with improved confocality and signal to noise.

Methods and Results: We recorded Ca²⁺ transients from cardiac ventricular myocytes isolated from rabbit hearts. Action potentials were produced by electric stimulation, and rapid solution changes were used to modify the L-type Ca²⁺ current. After the upstroke of the Ca²⁺ transient, LCSs were detected which had increased amplitude compared with diastolic Ca²⁺ sparks. LCS are triggered by both L-type Ca²⁺ channel activity during the action potential plateau, as well as by the increase of cytosolic Ca²⁺ associated with the Ca²⁺ transient itself. Importantly, a mismatch between sarcoplasmic reticulum load and L-type Ca²⁺ trigger can increase the number of LCS. The likelihood of triggering an LCS also depends on recovery from refractoriness that appears after prior activation. Consequences of LCS include a reduced rate of decline of the Ca²⁺ transient and, if frequent, formation of microscopic propagating Ca²⁺ release events (Ca²⁺ ripples). Ca²⁺ ripples resemble Ca²⁺ waves in terms of local propagation velocity but spread for only a short distance because of limited regeneration.

Conclusions: These new types of Ca²⁺ signaling behavior extend our understanding of Ca²⁺-mediated signaling. LCS may provide an arrhythmogenic substrate by slowing the Ca²⁺ transient decline, as well as by amplifying maintained Ca²⁺ current effects on intracellular Ca²⁺ and consequently Na⁺/Ca²⁺ exchange current.

基本原理：在心肌细胞中^{Ca 2+释放后，Ca 2+}火花开始不应期的发展会在动作电位平台期^{抑制进一步的 Ca 2+释放。}然而，最初未激活或过早从不应^{期恢复的 Ca 2+}释放位点可能会在动作电位后期^{释放 Ca 2+并改变细胞范围的 Ca 2+}瞬态。

目的：使用具有改善的共焦性和信噪比的快速共焦线扫描研究在完整的离体心肌细胞^{中晚期 Ca 2+}火花 (LCS) 活动的可能性

方法和结果：我们记录了从兔心脏分离的心肌细胞的Ca ^2+瞬变。通过电刺激产生动作电位，并使用快速溶液变化来改变L型Ca ²⁺电流。在Ca ^{2+瞬变的上行冲程之后，检测到与舒张Ca 2+}火花相比振幅增加的LCSLCS 由动作电位平台期间的L 型 Ca ²⁺通道活性以及与 Ca ²⁺瞬变本身^{相关的胞质 Ca 2+的增加触发。}重要的是，肌质网负荷与 L 型 Ca ^2+不匹配触发可以增加LCS的数量。触发 LCS 的可能性还取决于从先前激活后出现的不应期的恢复。^{LCS 的后果包括 Ca 2+}瞬态下降率降低，如果频繁，则形成微观传播的 Ca ²⁺释放事件（Ca ²⁺波纹）。Ca ²⁺波纹在局部传播速度方面类似于 Ca ²⁺波，但由于再生有限，只能传播很短的距离。

结论：这些新型 Ca ²⁺信号传导行为扩展了我们对 Ca ²⁺介导的信号传导的理解。^{LCS 可以通过减缓 Ca 2+}瞬时下降以及通过放大维持的 Ca ²⁺电流对细胞内 Ca ²⁺的影响以及因此 Na ⁺ /Ca ²⁺交换电流来提供致心律失常底物