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.

Keywords

• Experimental, glutamine, neuromuscular, sepsis

References

1. 1. Ahlbeck K, Fredriksson K, Rooyackers O, Måbäck G, Remahl S, Ansved T, et al. Signs of critical illness polyneuropathy and myopathy can be seen early in the ICU course. Acta Anaesthesiol Scand 2009;53:717-23. [CrossRef]
2. 2. Cankayali I, Dogan YH, Solak I, Demirag K, Eris O, Demirgoren S, et al. Neuromuscular deterioration in the early stage of sepsis in rats. Critical Care 2007;11:R1. [CrossRef]
3. 3. Cankayali I, Dogan YH, Solak I, Eris O, Demirgoren S, Moral AR. Effects of IgM-enriched immunoglobulin and fluid replacement on nerve conduction velocity in experimental sepsis. Turkish Journal of Trauma & Emergency Surgery 2010; Ulus Travma Acil Cerrahi Derg 2010;16:9-14.
4. 4. Brough W, Horne G, Blount A, Irving MH, Jeejeebhoy KN. Effects of nutrient intake. surgery. sepsis. and long term administration of steroids on muscle function. Br Med J 1986;293:983-8. [CrossRef]
5. 5. Boczkowski J, Dureuil B, Branger C, Pavlovic D, Murciano D, Pariente R, et al. Effects of sepsis on diaphragmatic function in rats. Am Rev Respir Dis 1988;138:260-5. [CrossRef]
6. 6. Ricks E. Critical illness polyneuropathy and myopathy: a review of evidence and the implications for weaning from mechanical ventilation and rehabilitation. Physiotherapy 2007;93:151-6. [CrossRef]
7. 7. Burnham EL, Moss M, Ziegler TR. Myopathies in critical illness: Characterization and nutritional aspects. J Nutr 2005; 1818S-23S.
8. 8. Latronico N, Shehu I, Seghelini E. Neuromuscular sequelae of critical illness. Curr Opin in Crit Care 2005;11:381-90. [CrossRef]

9. 9. Vermeulen MA, van de Poll MC, Ligthart-Melis GC, Dejong CH, van den Tol MP, Boelens PG, et al. Spesific amino acids in critically ill patient-Exogenous glutamine/arginine: A common denominator. Crit Care Med 2007;35:S568-S76. [CrossRef]
10. 10. Vesali RF, Klaude M, Rooyackers O, Wernerman J. Amino acid metabolism in leg muscle after an endotoxin injection in healthy volunteers. Am J Physiol Endocrinol Metab 2005;E360-E4. [CrossRef]
11. 11. Häussinger D, Lang F, Gerok W. Regulation of cell function by the cellular hydration state. Am J Physiol 1994;67:E343-55.
12. 12. Roth E, Oehler R. Hypothesis: Muscular glutamine deficiency in sepsis- a necessary step for a hibernation-like state. Nutrition 2010;26:571-4. [CrossRef]
13. 13. Otero-Anton E, Gonzalez-Quintela A, Lopez-Soto A, LopezBen S, Llovo J, Perez LF. Cecal ligation and puncture as a model of sepsis in the rat: influence of the puncture size on mortality, bacteremia, endotoxemia and tumor necrosis factor alpha levels. Eur Surg Res 2001;33:77-9. [CrossRef]
14. 14. Ritter C, Andrades M, Frota Junior ML, Bonatto F, Pinho RA, Polydoro M, et al. Oxidative parameters and mortality in sepsis induced by cecal ligation and perforation. Intensive Care Med 2003;29:1782-9. [CrossRef]
15. 15. Bolton CF. Evidence of neuromuscular dysfunction in the early stage of the systemic inflammatory responce syndrome. Intensive Care Med 2000;26:1179-80. [CrossRef]
16. 16. Bolton CF. Neuromuscular manifestations of critical illness. Muscle Nerve 2005;32:140-63. [CrossRef]
17. 17. Tennilä A, Salmi T, Pettilä V, Roine RO, Varpula T, Takkunen O. Early signs of critical illness polyneuropathy in ICU patients with systemic inflammatory response syndrome or sepsis. Intensive Care Med 2000;26:1360-3. [CrossRef]
18. 18. Cuddon PA, Murray M, Kraus K. Electrodiagnosis. In: Saltter DH, editor. Textbook of Small Animal Surgery Volume II, 3rd ed. Philadelphia; Saunders 2003:1108-17.
19. 19. Bolton CF. Gilbert JJ. Hahn AF, Sibbald WJ. Polyneuropathy in critically ill patients. J Neurol Neurosurg Psychiatry 1984; 47:1223-31. [CrossRef]
20. 20. Zochodne DW, Bolton CF, Wells GA, Gilbert JJ, Hahn AF, Brown JD et al. Critical illness polyneuropathy. A complication of sepsis and multiple organ failure. Brain 1987;110:819-41. [CrossRef]
21. 21. Bolton CF. Sepsis and the systemic inflammatory response syndrome: neuromuscular manifestations. Crit Care Med 1996;24:1408-16. [CrossRef]
22. 22. Routsi C, Gerovasili V, Vasileiadis I, Karatzanos E, Pitsolis T, Tripodaki E, et al. Electrical muscle stimulation prevents critical illness polyneuromyopathy: a randomized parallel intervention trial. Crit Care 2010;14:R74. [CrossRef]
23. 23. Moss M, Yang M, Macht M, Sottile P, Gray L, McNulty M, et al. Screening for critical illness polyneuromyopathy with single nerve conduction studies. Intensive Care Med 2014;40:683-90. [CrossRef]
24. 24. Plank LD, Connoly AB, Hill AG. Sequential changes in the metabolic response in severely septic patients during the first 23 days after onset of peritonitis. Ann Surg 1998;228:146-58. [CrossRef