Dresdner K P, Kline R P
Biophys J. 1985 Jul;48(1):33-45. doi: 10.1016/S0006-3495(85)83758-9.
The extracellular free [Ca++] in frog ventricular muscle strips was monitored using single-barrel calcium ion-selective microelectrodes. During trains of repetitive stimulation, a heart rate-dependent, sustained fall (depletion) of the extracellular free [Ca++] occurs, which is most likely a consequence of net Ca++ influx into ventricular cells. The magnitude of the [Ca++]0 depletion increases for higher Ringer's solution [Ca++], and is reversibly blocked by manganese ion. Prolonged repetitive field stimulation (20-30 min) activates additional cellular Ca++ efflux, which can balance the additional Ca++ influx caused by stimulation, resulting in abolition of extratrabecular [Ca++]0 depletion in 20-30 min, and hence zero net transmembrane Ca++ flux at steady state. In the poststimulation period of quiescence, cellular Ca++ efflux persists and causes an elevation (accumulation) of the extracellular free [Ca++]. From these [Ca++]0 depletions, quantitative estimates for the net transmembrane Ca++ flux were derived using an analytical solution to the diffusion equation. In the highest Ringer's solution [Ca++] used (1 mM) the calculated net increase of the total intracellular calcium per beat was 6.5 +/- 1.4 mumol/l of intracellular space. This corresponds to an average net transmembrane Ca++ influx of 0.81 +/- 0.17 pmol/cm2/s during the 800-ms action potential. In lower bath [Ca++] the net transmembrane [Ca++] flux was proportionately reduced.
使用单管钙离子选择性微电极监测青蛙心室肌条中的细胞外游离[Ca++]。在重复刺激序列期间,细胞外游离[Ca++]会出现与心率相关的持续下降(耗竭),这很可能是Ca++净流入心室细胞的结果。对于较高的任氏液[Ca++],[Ca++]0耗竭的幅度会增加,并且会被锰离子可逆性阻断。长时间的重复场刺激(20 - 30分钟)会激活额外的细胞Ca++外流,这可以平衡刺激引起的额外Ca++内流,导致在20 - 30分钟内小梁外[Ca++]0耗竭消失,从而在稳态时跨膜Ca++净通量为零。在刺激后的静息期,细胞Ca++外流持续存在,并导致细胞外游离[Ca++]升高(积累)。根据这些[Ca++]0耗竭情况,利用扩散方程的解析解得出跨膜Ca++净通量的定量估计值。在所使用的最高任氏液[Ca++](1 mM)中,计算得出每次心跳时细胞内总钙的净增加量为6.5±1.4 μmol/l细胞内空间。这对应于在800毫秒动作电位期间平均跨膜Ca++内流为0.81±0.17 pmol/cm2/s。在较低的浴液[Ca++]中,跨膜[Ca++]通量相应降低。