Résumé :
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Communication n° 457 Introduction : Critical illness polyneuropathy (CIP) remains to be delineated since it includes several nervous and muscular entities occurring after a sepsis in critically ill patients. Few data are available on the cellular mechanisms leading to this neuromuscular dysfunction. The aim of this study was to measure the muscular mechanical properties of the extensor digitorum longus (EDL) on a model of CIP induced by a chronic peritonitis in the rat. Methods : Two groups of 20 Wistar rats were submitted either to a chronic peritonitis (septic group) or no surgical procedure (control group). The effects of the chronic sepsis were assessed on day 14 on EDL by stimulation of distal sciatic nerve. The following measurements were then done: i) isometric contraction, tension-length relationship, a 2 minute fatigue test ; and ii) function of motor end plate by monitoring curarisation and decurarisation using the train of four technique after administration of 1mg.kg-1 of atracurium. Results : Optimal length was obtained for a 32% increase of the initial length for control while it was reached for a 40% increase (p<0.05) in septic rats. Table 1 summarises contractile indices of EDL, (*) denotes p<0.05 from the other groups. Tetanic stimulation showed a higher summation in the septic rats with a maximal tension of 92g at 15s of tetanus and 71g for control (p<0.05). Fatigue index was 0.23 Æ 0.11 in septic group and 0.59 Æ 0.19 in control (p<0.05). Curarisation kinetics are summarised in table 2. Conclusions : Atrophy may account for the decreased force. Shorter delay in contraction and relaxation in the septic group may be explained by a higher cytosolic concentration of calcium as shown by Bolton and/or higher sensitivity for calcium when compared to non septic animals (Belson et al.); Curarisation kinetics showing a quicker curarisation may be explained by an increased pharmacodynamy with a shorter delivery of the muscular blocking agent to the end plate by means of an increased cardiac output. The shorter decurarisation is in agreement with the litterature and may be explained by an upregulation of acetyl choline receptors with modified electrophysiologic properties. Table 1 Maximal tension Contraction time Time to half relaxation Septic 29,9 Æ 5,4 * 17,3 Æ 2,3 * 11 Æ 2,4 * Control 44 Æ 10 29 Æ 6,6 52 Æ 11 Table 2 Curarisation (s) Decurarisation (min) T4/T1 < 25% recovery T4/T1 > 75% Septic 36,7 * Æ 9,6 12,6 * Æ 5,7 22,9 * Æ 8,6 Control 54,6 Æ 1,7 22,3 Æ 2 47,2 Æ 1,2
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