Neuromuscular Dysfunction in Experimental Sepsis and Glutamine

Abstract

Background: Electrophysiological studies show thatcritical illness polyneuromyopathy appears in the earlystage of sepsis before the manifestation of clinical findings.The metabolic response observed during sepsiscauses glutamine to become a relative essential aminoacid.Aims: We aimed to assess the changes in neuromusculartransmission in the early stage of sepsis after glutaminesupplementation.Study Design: Animal experimentation.Methods: Twenty male Sprague-Dawley rats wererandomized into two groups. Rats in both groups weregiven normal feeding for one week. In the study group,1 g/kg/day glutamine was added to normal feeding byfeeding tube for one week. Cecal ligation and perforation(CLP) surgery was performed at the end of oneweek. Before and 24 hours after CLP, compound muscleaction potentials were recorded from the gastrocnemiusmuscle.Results: Latency measurements before and 24 hoursafter CLP were 0.68±0.05 ms and 0.80±0.09 ms in thecontrol group and 0.69±0.07 ms and 0.73±0.07 ms inthe study group (p