doi:10.1016/j.expneurol.2007.01.006 
Copyright © 2007 Elsevier Inc. All rights reserved.
Effects of chronic sepsis on rat motor units: Experimental study of critical illness polyneuromyopathy
Fabrice Rannoua, Jean-Pierre Penneca, Benoît Rossignolb, Julie Morelc, Germaine Dorangec, Charles Arvieuxb, Maxime Giouxa and Marie-Agnès Giroux-Metgesa, 
, 
aLaboratoire de Physiologie, Faculté de Médecine de Brest, CS 93837, 29238 BREST Cedex 3, France
bDépartement d’Anesthésie, Centre Hospitalier Universitaire de Brest, 29609 BREST Cedex, France
cLaboratoire de Culture Cellulaire, Institut de Synergie des Sciences et de la Santé, Centre Hospitalier Universitaire de Brest, 29609 BREST Cedex, France
Received 25 August 2006;
revised 14 December 2006;
accepted 5 January 2007.
Available online 13 January 2007.
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Abstract
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.
Keywords: Critical illness polyneuromyopathy; Chronic sepsis; Motor unit; Rat
Fig. 1. (A) Simultaneous recordings of (top to bottom) (1) muscle force twitch, (2) electrical muscle activity and (3) electrical nerve activity, after a single stimulating pulse of a ventral root filament containing only one motor axon to the soleus muscle. Time of stimulation (St) appears as an artefact at the beginning of nerve recording. Nerve action potential is pointed out by the arrow. Muscle action potential is observed on muscle electrodes (bipolar recording) and also on nerve electrode (monopolar recording) because of its important voltage (mV). Different latencies are measured as described in Methods. (B) Enlarged record of the same action potentials on muscle (1) and nerve (2).
Fig. 2. Mean and SEM (vertical bars) of tetanic forces for each motor unit type, obtained during successive 0.7-s stimulation bursts of stable frequency. Forces measured at each frequency, between 10 and 150 Hz, are expressed in percentage of the maximal tetanic force of this motor unit, usually obtained during the 100-Hz burst.
Fig. 3. Example of fatigue recordings corresponding to the Burke's protocol (first and 120th tetanus superimposed). (A) Control slow MU; (B) control fast MU; (C) septic MU. Lower trace: stimulations at 40 Hz lasting for 330 ms.
Table 1.
Weight loss and decrease in mean cross-sectional area (CSA) of skeletal muscle fibers induced by sepsis
Body weights are expressed as mean ± SEM before cecal ligation (basal weight) and 7 days after (final weight) for the septic and control group. The weight variation (Δweight) measured during the 7 days of observation is expressed as percentage. For each rat group, the number of cells whose CSA was measured is indicated in brackets. *p < 0.05, **p < 0.001.
Table 2.
Twitch and tetanus parameters of single motor units
Mechanical parameters of a single twitch contraction (peak force, contraction time, half relaxation time), maximal contraction force obtained during tetanic stimulation, and fatigability index corresponding to the percentage of initial force remaining at the end of the Burke's test. All parameters are expressed by mean ± SEM. Significant difference from control slow MU: *p < 0.05.
Table 3.
Latencies (ms) measured on polygraphic record (Fig. 1) after a single twitch stimulation and nervous conduction velocities (m s− 1) of single motor units (MU)
Stimulation–nerve AP: latency between stimulation and nerve action potential appearance (nerve AP), nerve AP–muscle AP: latency between nerve action potential appearance and muscle action potential appearance (muscle AP), muscle AP–beginning of contraction: latency between muscle action potential appearance and beginning of contraction, stimulation–beginning of contraction: latency between stimulation and beginning of contraction. All parameters are expressed as mean ± SEM. *Significant difference from control slow MU (p < 0.05).
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