Neuromuscular Dysfunction in Experimental Sepsis and Glutamine.

Abstract:

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.

journal_name

Balkan Med J

journal_title

Balkan medical journal

authors

Çankayalı İ,Boyacılar Ö,Demirağ K,Uyar M,Moral AR

doi

10.5152/balkanmedj.2016.140483

subject

Has Abstract

pub_date

2016-05-01 00:00:00

pages

267-74

issue

3

eissn

2146-3123

issn

2146-3131

pii

bmj-33-3-267

journal_volume

33

pub_type

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