Optical measurements of transmembrane potential changes during electric field stimulation of ventricular cells.
Optical measurements of transmembrane potential changes during electric field stimulation of ventricular cells.
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心室细胞电场刺激期间跨膜电位变化的光学测量。
DOI：
10.1161/01.res.72.2.255
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发表时间：
1993
影响因子：
20.1
通讯作者：
Ideker,RE
中科院分区：
文献类型：
--
作者：
Knisley,SB;Blitchington,TF;Hill,BC;Grant,AO;Smith,WM;Pilkington,TC;Ideker,RE
我们评估了在细胞不应期给予除颤强度电击时，分离的兔心室肌细胞末端跨膜电位的变化。刺激心肌细胞(S1脉冲)以产生动作电位。然后以50毫秒的S1-S2间隔给予电场为20 V/cm或40 V/cm的恒场冲击(S2脉冲)。用电位染料(di-4-ANEPPS)对细胞进行染色，并用激光照射面对S2阳极或阴极的细胞末端，同时记录荧光。在S2过程中，面向S2阴极的细胞端胞内变得更阳性，而面向S2阳极的细胞端变得更负。在每一次记录中，相对于S1诱导的动作电位(APA)的幅度(即，增量Vm/APA)，确定S2诱导的细胞末端跨膜电位的变化(增量Vm)。在含4.5 mM钾的Tyrode‘s溶液中，40 V/cm S_2的V_m/A_a在S_2阴极端为1.36+/-0.34，在S_2阳极端为-1.65+/-0.61(n=9)。对于20V/cm S_2，正对着S_2阴极端的V_m/APA为0.61+/-0.33，向S_2阳极端为-0.71+/-0.33(n=6)。20 mM丁二酮肟对DVm/APA无明显影响。这些结果表明，在S2期间，细胞末端出现了较大的增量Vm值。假设标称APA为130 mV，则计算的增量Vm分别为177 mV和-214 mV(40V/cmS2)和79 mV和-93 mV(20V/cmS2)。增量Vm与细胞大小(r>；OR=0.95)相关，并与S2电场强度乘以细胞长度的一半到27%以内的预测值一致。当钾浓度增加到20 mM时，40V/cmS_2时，正对着S_2阴阳极的电池端的ΔVm/P_(Apa)分别增加了85%和67%(n=9，p&t；0.005对4.5 mM K)，这与P_(Apa)的降低是一致的。因此，在细胞外钾正常或升高的情况下，除颤型刺激过程中细胞末端的跨膜电位变化足够大，足以激活或恢复电压依赖的离子通道，并可能产生与除颤相关的效应。
We evaluated transmembrane potential changes at the ends of isolated rabbit ventricular myocytes during defibrillation-strength shocks given in the cellular refractory period. The myocytes were stimulated (S1 pulse) to produce an action potential. Then a constant-field shock (S2 pulse) with an electric field of 20 or 40 V/cm was given at an S1-S2 interval of 50 msec. The cells were stained with potentiometric dye (di-4-ANEPPS), and the cell end facing the S2 anode or cathode was illuminated with a laser while the fluorescence was recorded. During S2, the cell end facing the S2 cathode became more positive intracellularly, whereas the cell end facing the S2 anode became more negative intracellularly. The S2-induced transmembrane potential change at the cell end (delta Vm) was determined relative to the amplitude of the S1-induced action potential (APA) in each recording (i.e., delta Vm/APA). In Tyrode's solution containing 4.5 mM potassium, delta Vm/APA for 40-V/cm S2 was 1.36 +/- 0.34 at the cell end facing the S2 cathode and -1.65 +/- 0.61 at the cell end facing the S2 anode (n = 9). For the 20-V/cm S2, delta Vm/APA was 0.61 +/- 0.33 at the cell end facing the S2 cathode and -0.71 +/- 0.33 at the cell end facing the S2 anode (n = 6). The delta Vm/APA was not significantly influenced by 20 mM diacetyl monoxime. These results indicate that large delta Vm values occurred at the ends of the cells during S2. The calculated values of delta Vm, assuming a nominal APA of 130 mV, were 177 and -214 mV for the 40-V/cm S2 and 79 and -93 mV for the 20-V/cm S2. The delta Vm was correlated with cell size (r > or = 0.95) and agreed with values predicted by the S2 electric field strength multiplied by half of the cell length to within 27%. When the potassium concentration was increased to 20 mM, delta Vm/APA for 40 V/cm S2 increased 85% and 67% at the cell ends facing the S2 cathode and anode, respectively (n = 9, p < 0.005 versus 4.5 mM potassium), consistent with reduced APA. Thus, with normal or elevated extracellular potassium, transmembrane potential changes at the ends of cells during defibrillation-type stimulation are large enough to produce activation or recovery of voltage-dependent ion channels and may produce the effects responsible for defibrillation.