Fink R, Wettwer E
Pflugers Arch. 1978 May 31;374(3):289-92. doi: 10.1007/BF00585607.
Voltage clamp experiments on frog sartorius muscle fibres suggest that the large increase in resting potassium conductance during metabolic exhaustion is due to a change in the gating of activated potassium channels to a permanently open state. gK in exhausted fibres is less sensitive to externally applied blockers as Zn2+ and 4-aminopyridine (4-AP) while TEA+, Rb+ and Ba2+ act similarly, both in normal and exhausted fibres. In addition, injection experiments provide evidence that TEA+ and 4-AP applied internally to normal fibres effectively block potassium outward current, whereas in exhausted fibres the block seems to be smaller. These results suggest modifications in the structure of the potassium channels during metabolic exhaustion.
对青蛙缝匠肌纤维进行的电压钳实验表明，代谢性疲劳期间静息钾电导的大幅增加是由于激活的钾通道门控转变为永久开放状态所致。疲劳纤维中的gK对外加阻滞剂（如Zn2+和4-氨基吡啶（4-AP））的敏感性较低，而TEA+、Rb+和Ba2+在正常纤维和疲劳纤维中的作用相似。此外，注射实验提供的证据表明，向正常纤维内部施加TEA+和4-AP可有效阻断钾外向电流，而在疲劳纤维中这种阻断作用似乎较小。这些结果表明，代谢性疲劳期间钾通道的结构发生了改变。
