Eickhorn R, Kopf M, Stadler R, Antoni H
Physiologisches Institut der Universitaet Freiburg, Federal Republic of Germany.
Muscle Nerve. 1988 Sep;11(9):945-52. doi: 10.1002/mus.880110907.
High-voltage condenser discharges exerting a field strength of up to 1000 V/cm (discharge time constant 0.24-8 msec) applied to isolated sciatic frog nerve lead to disturbances of the propagation of action potentials including transient complete block of conduction. Such conduction disturbances are normally reversible within minutes. Inhibition of the activity of the membrane-bound Na+-K+ATPase prevents the recovery from conduction block. Withdrawal of external Ca2+ also prevents recovery, whereas blockade of protein synthesis by cycloheximide has no influence. The velocity of recovery depends on the temperature, with temperature coefficients (Q10) from 1.31 to 1.84 between 2 degrees and 30 degrees C. Transmission electron microscopy of nerves subjected to strong discharges shows alterations of the myelin sheath (splitting and cleft formation) which are, however, not specific for this mechanism of injury. No alterations are seen in the region of the free axoplasmic membrane of the node of Ranvier or in organelles. The results suggest a breakdown of the transmembrane ionic gradient causing the conduction disturbance.
对离体的蛙坐骨神经施加高达1000 V/cm的场强（放电时间常数为0.24 - 8毫秒）的高压电容放电，会导致动作电位传播紊乱，包括传导的短暂完全阻滞。这种传导紊乱通常在几分钟内是可逆的。抑制膜结合的Na⁺ - K⁺ATP酶的活性会阻止从传导阻滞中恢复。去除细胞外Ca²⁺也会阻止恢复，而环己酰亚胺对蛋白质合成的阻断则没有影响。恢复速度取决于温度，在2℃至30℃之间温度系数（Q10）为1.31至1.84。对经受强放电的神经进行透射电子显微镜检查显示髓鞘有改变（分裂和裂隙形成），然而，这并非这种损伤机制所特有的。在郎飞结的游离轴突质膜区域或细胞器中未观察到改变。结果表明跨膜离子梯度的破坏导致了传导紊乱。
