TNF[alpha] increases resting potential in isolated fibres from rat peroneus longus by a PKC mediated mechanism: Involvement in ICU acquired polyneuromyopathy

• Published in: Cytokine (Philadelphia, Pa.) Vol. 56; no. 2; pp. 149 - 152
• Main Authors: Guillouet, Maite, Gueret, Gildas, Rannou, Fabrice, Giroux-Metges, Marie-Agnes, Gioux, Maxime, Arvieux, Charles C, Pennec, Jean-Pierre
• Format: Journal Article
• Language: English
• Published: Elsevier 01.11.2011
• Subjects: Life Sciences; Drug; Microelectrodes; drug effects/physiology; Rats; drug effects; Tumor Necrosis Factor-alpha; Skeletal; Animals; Membrane Potentials; Wistar; pharmacology; Female; Dose-Response Relationship; Muscle
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1016/j.cyto.2011.05.023

Our aim was to investigate the effect of TNF[alpha] on muscle resting potential (RP) and then in muscle excitability and to demonstrate another mechanism implicated in intensive care units (ICU) acquired polyneuromyopathy. Methods: Experiments were carried out on adult female Wistar rats. After isolation of muscle fibres from peroneus longus, influence of TNF[alpha] was tested on RP by using intracellular microelectrodes. Digoxin and chelerythrin were used to determine the mechanism of TNF[alpha] action. Results: First, we found that TNF[alpha] 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. Conclusions: We demonstrated that TNF[alpha] 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.