Orchard C H, Eisner D A, Allen D G
Nature. 1983;304(5928):735-8. doi: 10.1038/304735a0.
Contraction of cardiac muscle depends on a transient rise of intracellular calcium concentration ([Ca2+]i) which is initiated by the action potential. It has, however, also been suggested that [Ca2+]i can fluctuate in the absence of changes in membrane potential. The evidence for this is indirect and comes from observations of (1) fluctuations of contractile force in intact cells, (2) spontaneous cellular movements, and (3) spontaneous contractions in cells which have been skinned to remove the surface membrane. The fluctuations in force are particularly prominent when the cell is Ca2+-loaded, and have been attributed to a Ca2+-induced Ca2+ release from the sarcoplasmic reticulum. In these conditions of Ca2+-loading the normal cardiac contraction is followed by an aftercontraction which has been attributed to the synchronization of the fluctuations. The rise of [Ca2+]i which is thought to underlie the aftercontraction also produces a transient inward current. This current, which probably results from a Ca2+-activated nonspecific cation conductance, has been implicated in the genesis of various cardiac arrhythmias. However, despite the potential importance of such fluctuations of [Ca2+]i their existence has, so far, only been inferred from tension measurements. Here we present direct measurements of such oscillations of [Ca2+]i.
心肌收缩依赖于由动作电位引发的细胞内钙浓度（[Ca2+]i）的短暂升高。然而，也有人提出，在膜电位没有变化的情况下，[Ca2+]i也会波动。其证据是间接的，来自于以下观察结果：（1）完整细胞中收缩力的波动；（2）自发的细胞运动；（3）去除表面膜的“去皮”细胞中的自发收缩。当细胞加载钙时，力的波动尤为明显，这被归因于肌浆网中钙诱导的钙释放。在这些钙加载条件下，正常的心脏收缩之后会出现后收缩，这被归因于波动的同步化。被认为是后收缩基础的[Ca2+]i升高也会产生短暂的内向电流。这种电流可能由钙激活的非特异性阳离子电导产生，与各种心律失常的发生有关。然而，尽管[Ca2+]i的这种波动具有潜在的重要性，但到目前为止，其存在仅从张力测量中推断出来。在此，我们展示了对[Ca2+]i这种振荡的直接测量。
