Zhou X, Rollins D L, Smith W M, Ideker R E
Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.
J Cardiovasc Electrophysiol. 1995 Apr;6(4):252-63. doi: 10.1111/j.1540-8167.1995.tb00397.x.
The purpose of this investigation was to study the transmembrane potential changes (delta Vm) during extracellular electrical field stimulation.
Vm was recorded in seven guinea pig papillary muscles in a tissue bath by a double-barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 microns) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten S1 stimuli, an S2 shock field created by a 10-msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 +/- 0.1, 2.9 +/- 0.2, 6.1 +/- 0.6, and 8.8 +/- 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak delta Vm caused by the above four potential gradients were 21.1 +/- 8.2, 33.6 +/- 13.6, 49.9 +/- 24.2, and 52.3 +/- 28.0 mV (P < 0.05 among the four groups) for the shocks causing depolarization and 37.9 +/- 14.2, 56.6 +/- 16.4, 83.1 +/- 19.4, and 92.9 +/- 29.1 mV (P < 0.05 among the four groups) for the shocks causing hyperpolarization. Though delta Vm increased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 +/- 0.5 times that of depolarization when the shock polarity was reversed (P < 0.05). As potential gradients increased from 1.7 +/- 0.1 to 8.8 +/- 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 +/- 1.8 to 1.6 +/- 0.7 msec for depolarizing shocks and from 6.0 +/- 3.1 to 3.4 +/- 1.9 msec for hyperpolarizing shocks (P < 0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vm during the shock, i.e., initial hyperpolarization, than depolarization, followed again by hyperpolarization.
During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between approximately 2 and 9 V/cm.
本研究的目的是探讨细胞外电场刺激期间的跨膜电位变化（δVm）。
在组织浴槽中，用双管微电极记录7只豚鼠乳头肌的Vm，一个管尖置于细胞内，另一个管尖刚好位于细胞外，同时在浴槽两端施加电刺激。两个微电极尖端之间的短距离（15至30微米）以及尖端与刺激电极平行的排列方式消除了刺激伪迹。在施加10次S1刺激后，通过组织两侧1 cm处的刺激电极，在动作电位平台期或舒张期施加由10毫秒方波产生的S2刺激场。对于同一刺入点，施加四种场强分别为1.7±0.1、2.9±0.2、6.1±0.6和8.8±0.9 V/cm的刺激。每种刺激强度下均施加两种刺激极性。对于在动作电位平台期施加的刺激，上述四种电位梯度引起的δVm峰值大小，导致去极化的刺激分别为21.1±8.2、33.6±13.6、49.9±24.2和52.3±28.0 mV（四组间P<0.05），导致超极化的刺激分别为37.9±14.2、56.6±16.4、83.1±19.4和92.9±29.1 mV（四组间P<0.05）。虽然δVm随电位梯度增加而增大，但两者关系并非线性。当刺激极性反转时，超极化幅度是去极化幅度的1.9±0.5倍（P<0.05）。随着电位梯度从1.7±0.1增加到8.8±0.9 V/cm，去极化刺激时膜反应的时间常数从3.5±1.8显著降至1.6±0.7毫秒，超极化刺激时从6.0±3.1降至3.4±1.9毫秒（与去极化刺激相比，P<0.01）。对于在舒张期施加的刺激，超极化刺激在刺激期间引起Vm的三相变化，即初始超极化，然后去极化，随后再次超极化。
在动作电位平台期，膜反应不能用经典的被动RC膜模型表示。在舒张期，即使在由约2至9 V/cm电位梯度的刺激引起的超极化期间也会出现激活上升支。
