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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Format: | Article |
Language: | English |
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Galenos Publishing House
2016-06-01
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Series: | Balkan Medical Journal |
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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. |
first_indexed | 2024-04-10T12:20:30Z |
format | Article |
id | doaj.art-bd07fce898704ffda4874b075bac06a4 |
institution | Directory Open Access Journal |
issn | 2146-3123 2146-3131 |
language | English |
last_indexed | 2024-04-10T12:20:30Z |
publishDate | 2016-06-01 |
publisher | Galenos Publishing House |
record_format | Article |
series | Balkan Medical Journal |
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 |
work_keys_str_mv | AT ilkincankayalı neuromusculardysfunctioninexperimentalsepsisandglutamine AT ozdenboyacılar neuromusculardysfunctioninexperimentalsepsisandglutamine AT kubilaydemirag neuromusculardysfunctioninexperimentalsepsisandglutamine AT mehmetuyar neuromusculardysfunctioninexperimentalsepsisandglutamine AT aliresatmoral neuromusculardysfunctioninexperimentalsepsisandglutamine |