Head Injury: Metabolic, Nutritional, and Energy Considerations

Charrueau, Christine; Morio, Béatrice; Moinard, Christophe

doi:10.1007/978-0-387-92271-3_103

Cited by 2 publications

(3 citation statements)

References 66 publications

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“…These results agree with those of previous studies performed in septic rats, which clearly demonstrated that cysteine requirement was increased during sepsis (Malmezat et al, 2000). This may be related to an increase in glutathione synthesis (a major factor in oxidative defense during infection; Charrueau et al, 2010). Fibrinogen was lower and albumin was higher in the HI-EC group (vs HI), but we have no ready explanation for this unexpected finding.…”

Section: Discussionsupporting

confidence: 91%

“…These alterations are thought to be induced by the acutephase response, with synthesis of proinflammatory cytokines, and then synthesis of inflammatory proteins such as fibrinogen, along with gluconeogenesis and ureagenesis. This leads to muscle protein mobilization and induces a shift of amino acids from the periphery to the central organs, which explains the amino acid disturbances observed (see Charrueau et al, 2010 for a recent review). Interestingly, we observed that infection was associated with specific modifications such as decreased levels of sulfur amino acids (methionine and cysteine).…”

Section: Discussionmentioning

confidence: 95%

“…However, the cerebral lesions are accompanied by a systemic metabolic response (increased energy expenditure and muscle proteolysis, and development of a wasting syndrome), which rapidly leads to a state of malnutrition. The consequences are dysimmunity and septic episodes (Charrueau et al, 2010). The latter are recognized as inducing multiple disorders such as hemodynamic instability, and to worsen nutritional alterations and disturbances of hormonal patterns.…”

Section: Introductionmentioning

confidence: 99%

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In VivoBioluminescent Imaging of a New Model of Infectious Complications in Head-Injury Rats

Moinard

Butel

Bureau

et al. 2012

Journal of Neurotrauma

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Infectious complications are responsible for 10-25% of mortality in head-injured patients. In the present work we developed a model of infectious complications in head-injury rats using Escherichia coli (E. coli) with a stable copy of the lux operon, and monitored the infection in vivo by optical imaging. Rats were randomized into three groups: AL (healthy rats), HI (head-injury rats), and HI-EC (HI rats+single enteral bolus of E. coli, 1.3×10(9)/rat given 2 days after HI). Infection was evaluated with a camera at 2 and 6 h after E. coli challenge. Blood and organs were sampled to assess biological parameters. HI was associated with body weight loss, muscle atrophy, and plasma amino acid disturbances, in particular glutamine depletion (AL 919±37 versus HI 647±25 and HI-EC 717±20 μmol/L; p<0.05). In the HI-EC rats, the luminescence signal was observed at T+2 (mean [range]: 34,778 cpm [1617-2,918,810]), and was significantly decreased at T+6 (0 cpm [0-847,922]; p<0.05). Bacterial challenge was associated with a specific body weight loss and a decrease in gastrocnemius protein content, in alanine (AL 512±41 versus HI-EC 395±29 μmol/L; p<0.05), and in sulfur plasma amino acids. In conclusion, we propose a controlled model of HI with infectious complications characterized by specific metabolic alterations. Combined with the in vivo monitoring of the infection by bioluminescence, this model offers a valuable tool to evaluate specific strategies for HI patients.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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In VivoBioluminescent Imaging of a New Model of Infectious Complications in Head-Injury Rats

Moinard

Butel

Bureau

et al. 2012

Journal of Neurotrauma

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An Oligomeric Diet Limits the Response to Injury in Traumatic Brain-Injured Rats

Moinard

Delpierre

Loi

et al. 2013

Journal of Neurotrauma

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Adequate nutritional support is a major challenge in brain injury patients, because malnutrition cannot be reversed by standard enteral nutrition. We hypothesized that an oligomeric formula could improve nutritional status by restoring intestinal trophicity. Eighteen male Sprague-Dawley rats (300-330 g) underwent gastrostomy on day-7 (D-7) and traumatic brain injury (TBI) by hydraulic percussion (D0) and were then fed for 4 days with either a polymeric formula (Sondalis® HP, TBIP, n = 9), or an oligomeric formula (Peptamen® HN, TBIO, n = 9). In addition, a control group of healthy gastrostomized rats was fed the polymeric diet (control, n = 8). All rats were weighed daily. On D+4, the rats were euthanized. Blood was collected for plasma amino acid determination. Organs were removed and weighed. Intestinal morphometry was studied. Protein content was assessed on intestine and muscles. Enterobacterial translocation and dissemination were evaluated. Results were expressed as means ± SEM and compared using analysis of variance+Newman-Keuls test. TBI induced a significant decrease in whole body weight (TBIP vs. control, p < 0.05) that was totally blunted by the oligomeric diet (TBIP vs. TBIO, p < 0.01). Thymus weight significantly decreased after TBI (TBIP vs. control, p < 0.05) and was restored by the oligomeric formula (TBIO vs. TBIP, p < 0.05). Glutamine (GLN) concentration was improved by the oligomeric diet in both plasma (TBIO: 688 ± 19 vs. control: 591 ± 45 and TBIP: 615 ± 42 μmol/L, p < 0.05) and soleus muscle. These results show that the use of an oligomeric diet may limit response to injury after brain injury and could be a simple nutritional strategy in this setting.

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Head Injury: Metabolic, Nutritional, and Energy Considerations

Cited by 2 publications

References 66 publications

In VivoBioluminescent Imaging of a New Model of Infectious Complications in Head-Injury Rats

In VivoBioluminescent Imaging of a New Model of Infectious Complications in Head-Injury Rats

An Oligomeric Diet Limits the Response to Injury in Traumatic Brain-Injured Rats

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