Rannou Fabrice, Pennec Jean-Pierre, Rossignol Benoît, Morel Julie, Dorange Germaine, Arvieux Charles, Gioux Maxime, Giroux-Metges Marie-Agnès
Laboratoire de Physiologie, Faculté de Médecine de Brest, CS 93837, 29238 BREST Cedex 3, France.
Exp Neurol. 2007 Apr;204(2):741-7. doi: 10.1016/j.expneurol.2007.01.006. Epub 2007 Jan 13.
Critical illness polyneuromyopathy (CIP) leads to major muscle weakness correlated with peripheral nerve and/or muscle alterations. Because sepsis seems to be the main factor, we used an experimental model of chronic sepsis in rats to study the localization of the first alterations on isolated motor units of soleus muscle. Seven days of chronic sepsis leads to a decrease in muscle force and an increase in muscle fatigability. Muscle twitch contraction time is also slower and all the motor units exhibit a slow profile in septic rats. Motor axon conduction velocity remains normal. We observed a significant increase in the latency between nerve and muscle action potentials but no modifications in the electromechanical delay. The first action of sepsis on motor units seems to be a delayed trigger of muscle action potential along with a muscle weakness but without nerve conduction impairment.
危重病性多神经病和肌病（CIP）会导致严重的肌肉无力，这与周围神经和/或肌肉改变相关。由于脓毒症似乎是主要因素，我们使用大鼠慢性脓毒症实验模型来研究比目鱼肌单个运动单位最早出现改变的部位。七天的慢性脓毒症会导致肌肉力量下降和肌肉疲劳性增加。肌肉抽搐收缩时间也会变慢，并且在脓毒症大鼠中所有运动单位都呈现出慢波形态。运动轴突传导速度保持正常。我们观察到神经和肌肉动作电位之间的潜伏期显著增加，但机电延迟没有改变。脓毒症对运动单位的首要作用似乎是肌肉动作电位的触发延迟以及肌肉无力，但没有神经传导受损。
