Neuromuscular Dysfunction in Experimental Sepsis and Glutamine.
Balkan Med J
; 33(3): 267-74, 2016 May.
Article
en En
| MEDLINE
| ID: mdl-27308070
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. STUDYDESIGN:
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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Bases de datos:
MEDLINE
Tipo de estudio:
Clinical_trials
Idioma:
En
Revista:
Balkan Med J
Año:
2016
Tipo del documento:
Article
País de afiliación:
Turquía