摘要:

Purpose of reviewThis review will attempt to summarize recent clinical and experimental data on glutamine's use in critical illness. It will try to present the concept of glutamine as a ‘drug’ or ‘nutraceutical’, given in addition to standard nutritional support.Recent findingsGlutamine, traditionally considered to be a nonessential amino acid, is now considered as ‘conditionally essential’ following critical illness and injury. States of critical illness lead to significant decreases in plasma levels of glutamine and when this decrease is severe it has been correlated with increased mortality. Laboratory data have demonstrated numerous benefits of glutamine in experimental models of critical illness, including attenuated proinflammatory cytokine expression, improved gut barrier function, enhanced ability to mount a stress response, improved immune cell function, and decreased mortality. Over the last 10 years clinical trials of glutamine supplementation in critical illness have shown benefit with regard to mortality, length of stay, and infectious morbidity. However, data demonstrating a lack of benefit with glutamine supplementation in the critically ill have been presented as well. It appears that dose and route of administration clearly influence the benefit observed from glutamine administration, with high-dose, parenteral glutamine demonstrating an advantage over low-dose, enteral glutamine.SummaryHigh-dose or parenteral (>0.20-0.30 g/kg/day or ⩾30 g/day) glutamine appears to demonstrate the greatest potential for benefit in critically ill patients. No evidence of harm has been observed in studies conducted to date, thus further clinical trials utilizing glutamine as a pharmacologic supplement to standard nutrition are warranted.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewArginine, often found in immunonutrition regimens, is an important modulator of immune system activation. However, the mechanism of how arginine may be beneficial in immunonutrition is poorly understood. This review details the importance of arginine, its metabolism, and ultimately, its physiologic role in critically ill and immunocompromised patients.Recent findingsThe metabolism of arginine is determined by the expression of the arginine metabolizing enzymes inducible nitric oxide synthase and two arginase isoforms (arginase I and II). Inducible nitric oxide synthase is induced by T helper I cytokines (interleukin-1, tumor necrosis factor and γ-interferon), while arginases are induced by T helper II cytokines and other immune regulators such as interleukins 4, 10, and 13, transforming growth factor-β and prostaglandin E2. Endotoxin induces inducible nitric oxide synthase and arginases I and II. Arginase plays an important role in the production of ornithine, a precursor of proline and polyamines, both of which are necessary for cellular proliferation and wound healing. Arginase also induces nitric oxide synthase activity by competing for arginine availability in the extracellular environment, and producing polyamines, which may modulate macrophage activation. Through limitation of arginine availability in the extracellular environment, arginases also potentially regulate other ‘arginine-dependent’ immune functions such as T-lymphocyte activation, although this hypothesis remains to be proven.SummaryThe availability of arginine during critical illness may be regulated by arginase activity. Thus, arginase expression appears to be essential in the regulation of the cellular immune response and the inflammatory process during critical illness.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewIn recent years, evidence has mounted in favor of the antiinflammatory, immunomodulatory and cytoprotective effects of the simplest amino acid L-glycine. This article will focus on the recent findings about the responsible mechanisms of protection and review the beneficial effects of glycine in different disease states.Recent findingsGlycine protects against shock caused by hemorrhage, endotoxin and sepsis, prevents ischemia/reperfusion and cold storage/reperfusion injury to a variety of tissues and organs including liver, kidney, heart, intestine and skeletal muscle, and diminishes liver and renal injury caused by hepatic and renal toxicants and drugs. Glycine also protects against peptidoglycan polysaccharide-induced arthritis and inhibits gastric secretion and protects the gastric mucosa against chemically and stress-induced ulcers. Glycine appears to exert several protective effects, including antiinflammatory, immunomodulatory and direct cytoprotective actions. Glycine acts on inflammatory cells such as macrophages to suppress activation of transcription factors and the formation of free radicals and inflammatory cytokines. In the plasma membrane, glycine appears to activate a chloride channel that stabilizes or hyperpolarizes the plasma membrane potential. As a consequence, agonist-induced opening of L-type voltage-dependent calcium channels and the resulting increases in intracellular calcium ions are suppressed, which may account for the immunomodulatory and antiinflammatory effects of glycine. Lastly, glycine blocks the opening of relatively non-specific pores in the plasma membrane that occurs as the penultimate event leading to necrotic cell death.SummaryMultiple protective effects make glycine a promising treatment strategy for inflammatory diseases.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID