Neuromuscular Dysfunction in Experimental Sepsis and Glutamine

Background: Electrophysiological studies show that critical illness polyneuromyopathy appears in the early stage of sepsis before the manifestation of clinical findings. The metabolic response observed during sepsis causes glutamine to become a relative essential amino acid. Aims: We aimed to ass...

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Main Authors: İlkin Çankayalı, Özden Boyacılar, Kubilay Demirağ, Mehmet Uyar, Ali Reşat Moral
Format: Article
Language:English
Published: Galenos Publishing House 2016-06-01
Series:Balkan Medical Journal
Subjects:
Online Access:http://balkanmedicaljournal.org/text.php?lang=en&id=120
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author İlkin Çankayalı
Özden Boyacılar
Kubilay Demirağ
Mehmet Uyar
Ali Reşat Moral
author_facet İlkin Çankayalı
Özden Boyacılar
Kubilay Demirağ
Mehmet Uyar
Ali Reşat Moral
author_sort İlkin Çankayalı
collection DOAJ
description Background: Electrophysiological studies show that critical illness polyneuromyopathy appears in the early stage of sepsis before the manifestation of clinical findings. The metabolic response observed during sepsis causes glutamine to become a relative essential amino acid. Aims: We aimed to assess the changes in neuromuscular transmission in the early stage of sepsis after glutamine supplementation. Study Design: Animal experimentation. Methods: Twenty male Sprague-Dawley rats were randomized into two groups. Rats in both groups were given normal feeding for one week. In the study group, 1 g/kg/day glutamine was added to normal feeding by feeding tube for one week. Cecal ligation and perforation (CLP) surgery was performed at the end of one week. Before and 24 hours after CLP, compound muscle action potentials were recorded from the gastrocnemius muscle. Results: Latency measurements before and 24 hours after CLP were 0.68±0.05 ms and 0.80±0.09 ms in the control group and 0.69±0.07 ms and 0.73±0.07 ms in the study group (p<0.05). Conclusion: Since enteral glutamine prevented compound muscle action potentials (CMAP) latency prolongation in the early phase of sepsis, it was concluded that enteral glutamine replacement might be promising in the prevention of neuromuscular dysfunction in sepsis; however, further studies are required.
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spelling doaj.art-bd07fce898704ffda4874b075bac06a42023-02-15T16:15:29ZengGalenos Publishing HouseBalkan Medical Journal2146-31232146-31312016-06-0133326727410.5152/balkanmedj.2016.140483Neuromuscular Dysfunction in Experimental Sepsis and Glutamineİlkin Çankayalı0Özden Boyacılar1Kubilay Demirağ2Mehmet Uyar3Ali Reşat Moral4Department of Anesthesiology and Intensive Care, Ege University School of Medicine, İzmir, TurkeyDepartment of Anesthesiology and Intensive Care, Ege University School of Medicine, İzmir, TurkeyDepartment of Anesthesiology and Intensive Care, Ege University School of Medicine, İzmir, TurkeyDepartment of Anesthesiology and Intensive Care, Ege University School of Medicine, İzmir, TurkeyDepartment of Anesthesiology and Intensive Care, Ege University School of Medicine, İzmir, TurkeyBackground: Electrophysiological studies show that critical illness polyneuromyopathy appears in the early stage of sepsis before the manifestation of clinical findings. The metabolic response observed during sepsis causes glutamine to become a relative essential amino acid. Aims: We aimed to assess the changes in neuromuscular transmission in the early stage of sepsis after glutamine supplementation. Study Design: Animal experimentation. Methods: Twenty male Sprague-Dawley rats were randomized into two groups. Rats in both groups were given normal feeding for one week. In the study group, 1 g/kg/day glutamine was added to normal feeding by feeding tube for one week. Cecal ligation and perforation (CLP) surgery was performed at the end of one week. Before and 24 hours after CLP, compound muscle action potentials were recorded from the gastrocnemius muscle. Results: Latency measurements before and 24 hours after CLP were 0.68±0.05 ms and 0.80±0.09 ms in the control group and 0.69±0.07 ms and 0.73±0.07 ms in the study group (p<0.05). Conclusion: Since enteral glutamine prevented compound muscle action potentials (CMAP) latency prolongation in the early phase of sepsis, it was concluded that enteral glutamine replacement might be promising in the prevention of neuromuscular dysfunction in sepsis; however, further studies are required.http://balkanmedicaljournal.org/text.php?lang=en&id=120Experimentalglutamineneuromuscularsepsis
spellingShingle İlkin Çankayalı
Özden Boyacılar
Kubilay Demirağ
Mehmet Uyar
Ali Reşat Moral
Neuromuscular Dysfunction in Experimental Sepsis and Glutamine
Balkan Medical Journal
Experimental
glutamine
neuromuscular
sepsis
title Neuromuscular Dysfunction in Experimental Sepsis and Glutamine
title_full Neuromuscular Dysfunction in Experimental Sepsis and Glutamine
title_fullStr Neuromuscular Dysfunction in Experimental Sepsis and Glutamine
title_full_unstemmed Neuromuscular Dysfunction in Experimental Sepsis and Glutamine
title_short Neuromuscular Dysfunction in Experimental Sepsis and Glutamine
title_sort neuromuscular dysfunction in experimental sepsis and glutamine
topic Experimental
glutamine
neuromuscular
sepsis
url http://balkanmedicaljournal.org/text.php?lang=en&id=120
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AT ozdenboyacılar neuromusculardysfunctioninexperimentalsepsisandglutamine
AT kubilaydemirag neuromusculardysfunctioninexperimentalsepsisandglutamine
AT mehmetuyar neuromusculardysfunctioninexperimentalsepsisandglutamine
AT aliresatmoral neuromusculardysfunctioninexperimentalsepsisandglutamine