CHU Brest, Pôle Anesthésie Réanimation, Université de Brest, Faculté de Médecine et des Sciences de la Santé, EA 4326, Laboratoire de Physiologie, Brest, F-29200, France.
Cytokine. 2011 Nov;56(2):149-52. doi: 10.1016/j.cyto.2011.05.023. Epub 2011 Jul 6.
Our aim was to investigate the effect of TNFα on muscle resting potential (RP) and then in muscle excitability and to demonstrate another mechanism implicated in intensive care units (ICU) acquired polyneuromyopathy.
Experiments were carried out on adult female Wistar rats. After isolation of muscle fibres from peroneus longus, influence of TNFα was tested on RP by using intracellular microelectrodes. Digoxin and chelerythrin were used to determine the mechanism of TNFα action.
First, we found that TNFα induced a concentration dependent increase of muscle RP and that this mechanism, which was blocked by digoxin, was due to an effect on the Na/K ATPase. As it was also blocked by chelerythrin it was concluded that this effect was mediated by PKC activation of the Na/K ATPase.
We demonstrated that TNFα leads to a PKC mediated increase in muscle RP. Depolarization needed to reach the threshold voltage for muscle action potential should then be higher and this could be involved in the decrease in muscle excitability observed in acquired polyneuromyopathy.
我们的目的是研究 TNFα 对肌肉静息电位（RP）的影响，进而研究其对肌肉兴奋性的影响，并进一步揭示 ICU 获得性多发性神经病的另一种发病机制。
该实验在成年雌性 Wistar 大鼠上进行。腓肠肌纤维分离后，采用细胞内微电极检测 TNFα 对 RP 的影响。地高辛和Chelerythrine 用于确定 TNFα 作用的机制。
首先，我们发现 TNFα 诱导肌肉 RP 浓度依赖性增加，该机制可被地高辛阻断，这是由于对 Na/K-ATP 酶的影响所致。由于它也可被 Chelerythrine 阻断，因此可以得出结论，这种作用是通过 PKC 对 Na/K-ATP 酶的激活介导的。
我们证明 TNFα 导致肌肉 RP 的 PKC 介导增加。达到肌肉动作电位阈电压所需的去极化应该更高，这可能与获得性多发性神经病中观察到的肌肉兴奋性降低有关。
