Glutamine Supplements in the Critically Ill
Glutamine Supplements in the Critically Ill
复制标题
危重病人的谷氨酰胺补充剂
DOI:
10.1177/014107680409700904
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发表时间:
2004
影响因子:
17.3
通讯作者:
J. Powell
中科院分区:
文献类型:
--
作者:
R. D'Souza;J. Powell
Glutamine is a five-carbon neutral aminoacid containing two carboxyl groups one of which is bound to nitrogen, forming an amide group. It is the most abundant free aminoacid in the body.1 In the extracellular fluid it constitutes about 25% of the free aminoacid pool, in skeletal muscle more than 60%.1 A healthy 70 kg man contains 80 g of glutamine and the concentration of glutamine in his blood is 500– 700 mmol/L. Glutamine has numerous functions in normal physiology—for example, it acts as a precursor for protein synthesis; it provides the nitrogen for synthesis of arginine, purines, pyrimidines, nucleotides, glutathione and taurine (the last two being important antioxidants); and it transports amino-nitrogen to intestine, liver and kidney.1–3 With its involvement in renal ammoniagenesis it plays a key role in acid–base homoeostasis.2 Particularly reliant on glutamine as a fuel are the rapidly dividing cells of the gastrointestinal tract (enterocytes, colonocytes) and the immune system (lymphocytes, macrophages).3,4 Glutamine may affect stress-induced accumulation of extracellular fluid by changing the cellular hydration state.4 An increase in cellular hydration acts as an anabolic proliferative signal, whereas cell shrinkage is catabolic and anti-proliferative. Under normal circumstances glutamine is readily synthesized and stored in skeletal muscle whilst lesser amounts are produced in the liver, lungs and brain.1 Since it can be produced by the body it is regarded as a nonessential aminoacid. However, this does not apply to conditions of excessive organ/tissue demand such as sepsis and other states of catabolic stress declines greatly.4 In these circumstances, production of glutamine in the body is insufficient to meet the increased requirement by the gut, immune system, liver and kidneys.4 The demands are then met in part by protein breakdown in skeletal muscle, with release of large amounts of glutamine and glutamine becomes a conditionally essential aminoacid. CONSEQUENCES OF GLUTAMINE DEPLETION