glutamine/blæðing

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Administration of glutamine after hemorrhagic shock restores cellular energy, reduces cell apoptosis and damage, and increases survival.

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BACKGROUND Hemorrhagic shock causes a rapid depletion of adenosine triphosphate (ATP) and an increase of the terminal metabolite xanthine. Free radicals generated from xanthine oxidase play a major role in cell injury. Programmed cell death, apoptosis, is a major pathway causing reperfusion injury.

Glutamine administration during total parenteral nutrition protects liver adenosine nucleotides during and after subsequent hemorrhagic shock.

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BACKGROUND Glutamine supplementation of total parenteral nutrition (TPN) in stressed patients has been advocated. To determine whether glutamine supplementation affects the host response to conditions of stress, animals were given TPN with or without glutamine for 7 days. They were then subjected to

Cerebrospinal fluid glutamine in intracranial hemorrhage in the newborn.

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Cerebrospinal fluid concentration of glutamine was measured in 43 premature and mature babies suffering from intracranial hemorrhage. Compared with a control group of 38 infants we found elevated levels in all infants with intraparenchymal and subarachnoid hemorrhages. Two out of ten children with

Microdialysis patterns in subarachnoid hemorrhage patients with focus on ischemic events and brain interstitial glutamine levels.

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BACKGROUND This observational microdialysis (MD) study of 33 subarachnoid hemorrhage patients explores brain interstitial levels of glutamine, glutamate, lactate and pyruvate, and their relationship to clinical status and clinical course at the neurointensive care unit. METHODS The focus was on

Glycyl-L-glutamine [beta-endorphin-(30-31)] attenuates hemorrhagic hypotension in conscious rats.

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The profound hypotension caused by acute hemorrhage is thought to involve opioid peptide neurons. In this study, we tested whether glycyl-L-glutamine [Gly-Gln; beta-endorphin-(30-31)], a nonopioid peptide derived from beta-endorphin processing, prevents the cardiovascular depression induced by

Glutamine depletion in patients with Crimean-Congo Hemorrhagic Fever.

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Crimean-Congo hemorrhagic fever (CCHF) is a viral disease. There is not enough knowledge about plasma amino acid levels in CCHF. Therefore, we investigated of plasma amino acids levels in patients with CCHF and the association between the levels of these amino acids and disease severity. The plasma

[Protective effects of glutamine on the intestinal mucosal barrier in young rabbits under hemorrhagic shock].

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OBJECTIVE Glutamine (Gln) is now considered as conditionally essential amino acid with many biological activities. This study aimed to investigate whether it has protective effects on the intestinal mucosal barrier in young rabbits under hemorrhagic shock. METHODS Eighteen young rabbits aged 26 +/-

Glutamine supplementation does not prevent bacterial translocation after non-lethal haemorrhage in rats.

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OBJECTIVE To find out whether supplementation of an enteral diet with glutamine would reduce translocation of bacteria to mesenteric lymph nodes or blood after major haemorrhage in rats. METHODS Open randomised study. METHODS University departments of surgery and microbiology, Sweden. METHODS 49

Intestinal blood flow is restored with glutamine or glucose suffusion after hemorrhage.

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Intestinal blood flow has been shown to be impaired after resuscitated hemorrhagic shock. Enteral feeding has been proposed as an adjunct for preserving mucosal integrity and decreasing translocation-related morbidities during stress. The purpose of this study was to determine if an ileal mucosal

Glutamine dipeptides-supplemented parenteral nutrition reverses gut mucosal structure and interleukin-6 release of rat intestinal mononuclear cells after hemorrhagic shock.

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Glutamine is an essential substrate for gut mucosal structure, but the role for gut immune function is not fully known. To determine the effect on gut cytokine release in relation to bacterial translocation and gut morphology, a nonlethal hemorrhagic shock (30 min, 30 mmHg) was performed in male

Relationship between intracranial hemodynamics and microdialysis markers of energy metabolism and glutamate-glutamine turnover in patients with subarachnoid hemorrhage. Clinical article.

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OBJECTIVE The aim of this study was to explore the relationship between hemodynamics (intracranial and systemic) and brain tissue energy metabolism, and between hemodynamics and glutamate (Glt)-glutamine (Gln) cycle activity. METHODS Brain interstitial levels of lactate, pyruvate, Glt, and Gln were

Prevention of hemorrhagic shock-induced intestinal tissue injury by glutamine via heme oxygenase-1 induction.

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Hemorrhagic shock (HS) is an oxidative stress that causes intestinal tissue injury. Heme oxygenase 1 (HO-1) is induced by oxidative stress and is thought to play an important role in the protection of tissues from oxidative injury. We previously reported the ileum to be the most susceptible to

Alanine-glutamine dipeptide (AGD) inhibits expression of inflammation-related genes in hemorrhagic shock.

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BACKGROUND Inflammatory factors play an important role in the production of cellular damage after shock and reperfusion. Glutamine has been used to modulate the inflammatory response. Alanine-glutamine dipeptide (AGD) is a glutamine source. The hypothesis of the present study is that AGD given

Does intravenous glutamine prevent bacterial translocation in hemorrhagic shock?

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Bacterial translocation across the gut wall may be associated with insult to the latter. In this situation, intestinal flora can enter the blood stream and lymph nodes and be transported to other organs. Glutamine is a nonessential amino acid not presently included in total parenteral nutrition

Oral glutamine attenuates cyclophosphamide-induced oxidative stress in the bladder but does not prevent hemorrhagic cystitis in rats.

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Cyclophosphamide (CP) is widely used in the treatment of cancer and non-malignant disease states such as rheumatoid arthritis. Hemorrhagic cystitis is a major dose-limiting side effect of CP. The incidence of this side effect is related to the dosage and can be as high as 75%. Elimination of the

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