Characterization of the alteration of nutritional state in brain injury induced by fluid percussion in rats
Characterization of the alteration of nutritional state in brain injury induced by fluid percussion in rats
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DOI：
10.1007/s00134-004-2489-9
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发表时间：
2005-02-01
影响因子：
38.9
通讯作者：
Cynober, L
中科院分区：
文献类型：
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作者：
Moinard, C;Neveux, N;Cynober, L
目的：患有创伤性脑损伤（TBI）的患者经历快速体重减轻，负氮平衡和增强的全身蛋白质分解，蛋白质消耗导致发病率和死亡率增加。TBI的许多实验模型已被用于评估策略，以改善这些患者的结果，但营养状况还没有被认为是在迄今为止公布的实验，虽然这可能有很大的重要性，并影响与TBI模型获得的结果。本研究描述了TBI大鼠的高钙血症水平和营养状况。设计：24只雄性Wistar大鼠随机分为3组。TBI组大鼠麻醉后行液压冲击。配对喂养（PF）组是健康的，但与TBI组配对喂养。自由采食（AL）组是健康的，自由采食。该研究在TBI后10天内进行。测量和结果：TBI大鼠表现为明显的长期厌食、肾功能衰竭（肌酐清除率：AL 1.8 ± 0.2和PF 1.5 ± 0.1 vs. TBI 0.9 ± 0.1 l/24小时），厌食（整个研究期间食欲下降），肌原纤维蛋白水解增加（3-甲基组氨酸/肌酐比值（第2天：AL 36+/-1和PF 38+/-2 vs. TBI 54+/-5 mumol/mmol））和肠萎缩（回肠：AL 29.3+/-2.5和PF 28.7+/-1.1 vs. TBI 22.5+/-1.4 mg/cm）。此外，厌食症导致肌肉萎缩和氮平衡下降。上述代谢改变可增加发病率和死亡率。结论：通过大鼠中的液压冲击的TBI是再现在临床实践中观察到的代谢和营养改变的模型，并且适合于探索优化的营养支持的功效的进一步研究。
Objective: Patients suffering from traumatic brain injury (TBI) undergo rapid weight loss with negative nitrogen balance and enhanced whole-body protein breakdown, with protein wasting causing morbidity and increased mortality. Many experimental models of TBI have been used to evaluate strategies to improve the outcome of these patients, but nutritional status has not been considered in experiments published to date, although this may have great importance and influence the results obtained with TBI models. This study characterized the hypercatabolism level and nutritional status of TBI rats. Design: Twenty-four male Wistar rats were randomized into three groups. Rats from the TBI group were anesthetized and fluid percussion was applied. The pair-fed (PF) group was healthy but was pair-fed to the TBI group. The ad libitum (AL) group was healthy and fed ad libitum. The study was performed over 10 days post-TBI. Measurements and results: TBI in rats was characterized by remarkable long-lasting anorexia, renal failure (creatinine clearance: AL 1.8+/-0.2 and PF 1.5+/-0.1 vs. TBI 0.9+/-0.1 l/24 hour), anorexia (appetite depressed throughout the study), increased myofibrillar proteolysis (3-methylhistidine/creatinine ratio (day 2: AL 36+/-1 and PF 38+/-2 vs. TBI 54+/-5 mumol/mmol), and intestinal atrophy (ileum: AL 29.3+/-2.5 and PF 28.7+/-1.1 vs. TBI 22.5+/-1.4 mg/cm). In addition, anorexia led to muscular atrophy and decreased nitrogen balance. The metabolic alterations described above can increase morbidity and mortality. Conclusions: TBI by fluid percussion in rats is a model reproducing the metabolic and nutritional alterations observed in clinical practice and is suitable for further studies exploring the efficacy of optimized nutritional support.