Role of glutamine administration on T-cell derived inflammatory response after cardiopulmonary bypass

• Published in: Clinical nutrition (Edinburgh, Scotland) Vol. 28; no. 1; pp. 15 - 20
• Main Authors: Engel, J.M., Pitz, S., Mühling, J., Menges, T., Martens, F., Kwapisz, M., Hempelmann, G.
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01.02.2009; Elsevier
• Subjects: Aged; Biological and medical sciences; C-Reactive Protein - metabolism; Cardiopulmonary Bypass; Cytokines - biosynthesis; Cytokines - blood; Double-Blind Method; Feeding. Feeding behavior; Female; Fundamental and applied biological sciences. Psychology; Gastroenterology and Hepatology; Glutamine; Glutamine - administration & dosage; Glutamine - blood; Heart Diseases - blood; Heart Diseases - immunology; Heart Diseases - surgery; Humans; Inflammation - immunology; Inflammation - prevention & control; Infusions, Intravenous; Interleukin-1; Interleukin-6; Interleukin-8; Length of Stay; Male; Perioperative Care - methods; Postoperative Care; Postoperative Complications - prevention & control; Prospective Studies; T helper cells; Th1 Cells - drug effects; Th1 Cells - immunology; Th2 Cells - drug effects; Th2 Cells - immunology; Tumor necrosis factor-α; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Cardiopulmonary bypass; Interleukin-1; T helper cells; Tumor necrosis factor-α; Interleukin-8; Glutamine; Interleukin-6; Treatment; Bypass; Aminoacid; Surgery; T-Lymphocyte; Metabolic diseases; Inflammation
• ISSN: 0261-5614; 1532-1983; 1532-1983
• DOI: 10.1016/j.clnu.2008.08.007

Cardiac surgery provokes an inflammatory response for which the endothelium, the myocardium, and monocytes/macrophages are primarily responsible. T cells are altered in a different way whereby the pro-inflammatory pathway is suppressed. From the results of experimental studies it was concluded that glutamine (Gln) enhances the production of T-cell cytokines in conditions of Gln deprivation. The aim of this clinical study was to evaluate the role of a perioperative Gln infusion on intracellular inflammatory T-cell cytokine expression in patients undergoing elective cardiac surgery and to evaluate the effects on systemic inflammation, organ dysfunction and ICU length of stay. In this prospective, randomized, double-blind study, we included 78 patients (age level older than 70 years, ejection fraction less than 40%, or mitral valve replacement) undergoing elective cardiosurgery with cardiopulmonary bypass. We randomly assigned each subject to receive an infusion with either Gln (0.5 g/kg/day, group A) or an isonitrogenous, isocaloric, isovolemic nutritional solution (group B) or physiological NaCl 0.9% (group C, to eliminate an unspecific nutritional effect). We started the infusion after the induction of anesthesia with 1000 ml/24 h and maintained this state for 3 days. On the first postoperative day plasma Gln levels in group A were significantly increased (958 ± 331 μM) compared to group B (527 ± 105 μM) and group C (489 ± 104 μM), and remained higher until the third postoperative day. At the beginning and after surgery intracellular interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor-α levels in T cells showed no differences between the groups. Also, no differences could be observed with regard to C-reactive protein, SOFA score, heart and circulation support, postoperative ventilation time, and ICU length of stay. The elevation of Gln plasma levels as a result of 0.5 g/kg/day perioperative Gln infusion has no influence on the T-cell derived inflammatory response, indicating a sufficient supply of Gln. A Gln supplementation in cardiac surgery patients without a clear Gln deficiency seems not to affect the intracellular inflammatory T-cell cytokine expression.