Spontaneous Ca²⁺-transient (wave) generation in isolated cardiomyocytes is well established phenomenon which poses a lot of questions about myocardial excitability. Current studies of spontaneous Ca²⁺-activity in cardiac cells mainly relate to the kinetic characteristics, classification and simulation of Ca²⁺-events through ryanodine receptor (RyR) activity modeling. Here, for the first time we pay attention to the Ca²⁺-transients having stationary kinetics for correct estimation of the sarcoplasmic reticulum Ca²⁺ transport. In cardiomyocytes generating such type of Ca²⁺-transients, the averaged intracellular calcium ([Ca²⁺]_in) fluorescence practically does not change in time. Stationary Ca²⁺-transients are observed in different animal models (Wistar, SHR, ground squirrels) revealing a common cardiomyocyte phenomenon. They somewhat depend on external Ca²⁺ ([Ca²⁺]_ex) because the [Ca²⁺]_ex lowering to 1 μM in the presence of EGTA disrupts Ca²⁺-wave propagation. At the same time, spontaneous Ca²⁺-transients do not associated with the forward or reverse mode of Na⁺/Ca²⁺ exchanger (NCX), but partially modulated by the L-type Ca²⁺-channels. Among the sarcoplasmic reticulum targets, RyR and SERCA are crucial for Ca²⁺-wave generation and sustained self-oscillation activity. Analysis of the spontaneous wave kinetics reveals that both slopes of the rising wave front and the wave front decline are gradually changed during propagation, which well correlates with the RyR and SERCA activity, respectively. On the contrary, in the electrical field-stimulated myocytes, both slope factors are sharply changed corresponding to ‘all-or-nothing’ rule, which is fundamental principle for action potential in cardiomyocytes. Furthermore, stimulation of single cardiomyocyte using local electrode appears the deterioration in the [Ca²⁺]_in utilization from the cytosol, which limits the time of observation during the protocol. Obtained data suggest that stationary spontaneous Ca²⁺-transients occurring without actual myocellular excitation represent useful and precise tools for estimation of the sarcoplasmic reticulum Ca²⁺-transport.

在分离的心肌细胞中自发产生Ca ²⁺瞬态（波）是一种公认​​的现象，这引起了许多关于心肌兴奋性的问题。当前对心脏细胞中自发Ca ²⁺活性的研究主要涉及通过ryanodine受体（RyR）活性建模的动力学特征，Ca 2 ^+-事件的分类和模拟。在这里，我们第一次关注具有平稳动力学的Ca ²⁺瞬态，以正确估计肌质网Ca ^2+的转运。在心肌细胞中生成的Ca的这种类型²⁺ -transients，平均细胞内钙（[钙²⁺ ]_在）荧光几乎不会随时间变化。在不同的动物模型（Wistar，SHR，地松鼠）中观察到固定的Ca ²⁺瞬态现象，揭示了常见的心肌细胞现象。它们在某种程度上取决于外部Ca 2 ⁺（[Ca ²⁺ ] _ex），因为在存在EGTA的情况下[Ca ²⁺ ] _ex降低至1μM会破坏Ca 2 ^+-波的传播。同时，自发的Ca ²⁺瞬变与Na ⁺ / Ca ²⁺交换剂（NCX）的正向或反向模式无关，而是由L型Ca ^2+进行部分调节-频道。在肌质网靶标中，RyR和SERCA对于Ca ²⁺波的产生和持续的自激振荡活性至关重要。对自发波动力学的分析表明，上升波前和波前下降的斜率在传播过程中逐渐改变，分别与RyR和SERCA活性相关。相反，在电场刺激的心肌细胞中，两个斜率因子都急剧变化，对应于“全有或全无”规则，这是心肌细胞动作电位的基本原理。此外，使用局部电极刺激单个心肌细胞似乎会导致[Ca ²⁺ ]的降解_。胞浆的利用率，这限制了协议中观察的时间。获得的数据表明，在没有实际的肌细胞兴奋的情况下发生的稳态自发Ca ²⁺瞬变代表了评估肌浆网Ca ²⁺转运的有用且精确的工具。