谷氨酰胺对创伤大鼠细胞免疫功能的影响

目的：研究经口补充谷氨酰胺（Ｇｌｕｔａｍｉｎｅ，Ｇｌｎ）对创伤大鼠细胞免疫功能的影响。方法：采用闭合性创伤大鼠模型，通过补充或不补充谷氨酰胺，观察创伤后血浆、脾脏和肠系膜淋巴结细胞Ｇｌｎ含量，以及细胞免疫功能的动态变化。结果：创伤后补充Ｇｌｎ组（Ｇｌｎ组）血浆、脾脏和肠系膜淋巴结细胞Ｇｌｎ含量明显高于不补充Ｇｌｎ组（Ｎｏｎ－Ｇｌｎ组）；伤后大鼠脾脏和肠系膜淋巴结细胞的Ｔ淋巴细胞增殖反应下降，白介素－２（ＩＬ－２）生成减少，细胞膜ＩＬ－２受体（ＩＬ－２Ｒ）表达受抑，但Ｇｌｎ组动物的免疫抑制程度明显轻于Ｎｏｎ－Ｇｌｎ组。结论：经口补充Ｇｌｎ，能有效地提高创伤后血浆Ｇｌｎ水平，保持脾脏、淋巴结细胞及腹腔巨噬细胞内Ｇｌｎ正常含量，改善细胞免疫功能，减轻创伤后的免疫受抑程度。     

鱼油对感染大鼠肠粘膜的保护作用

目的：探讨膳食鱼油对感染机体小肠粘膜的保护作用。方法：将大鼠随机分为ＮＳ＋ＣＬＰ，ＦＯ＋ＣＬＰ及ＳＨＡＭ（假手术）三组（ｎ＝１５），术前分别灌食鱼油或等渗盐水１ｍｌ×３周，于ＣＬＰ后第二天采取标本检测血清ＴＮＦ、ＩＬ┐６、ＰＧＥ２浓度及小肠谷氨酰胺（Ｇｌｎ）含量，并用ＲＴ┐ＰＣＲ方法测定小肠粘膜ＴＮＦｍＲＮＡ的含量。结果：ＮＳ＋ＣＬＰ组大鼠血清ＴＮＦ、ＩＬ┐６、ＰＧＥ２水平明显高于ＳＨＡＭ组（Ｐ＜０．０１），小肠粘膜Ｇｌｎ含量显著减少（０．２８±０．１１ｖｓ０．９９±０．２１，Ｐ＜０．０１），而ＴＮＦｍＲＮＡ表达显著升高（Ｐ＜０．０１）。与之相比，灌食ＦＯ大鼠血清ＴＮＦ、ＩＬ┐６、ＰＧＥ２水平则有不同程度的下降，而小肠粘膜Ｇｌｎ含量明显高于ＮＳ＋ＣＬＰ组，同时，小肠粘膜ＴＮＦｍＲＮＡ的表达显著降低（Ｐ＜０．０１）。结论：鱼油能通过抑制花生四烯酸代谢产物的生成，改善小肠粘膜的血循环，或降低粘膜局部细胞因子的表达，阻断细胞因子对肠粘膜结构功能及细胞代谢的不利影响     

谷氨酸胺对创伤大鼠细胞免疫功能的影响

目的：研究经口补充谷氨酰胺对创伤大鼠细胞免疫功能的影响。方法：采用才合性创伤大鼠模型,通过补充或不补充谷氨酰胺,观察创伤后血浆、脾脏和肠系膜淋巴结细胞Ｇｌｎ含量,以及细胞免疫功能的动态变化,结果：创伤后补充Ｇｌｎ组血浆、脾脏和肠系膜淋巴结细胞Ｇｌｎ含量明显高于不补充Ｇｌｎ组;作在鼠脾脏和肠系膜淋巴结细胞的Ｔ淋巴细胞增殖反应下降,白介素－２（ＩＬ－２）生成减少,细胞膜ＩＬ－２受体（ＩＬ－２Ｒ）表达受     

表皮生长因子增强TPN对肠道免疫功能的影响

本文应用大鼠全肠外营养（ＴＰＮ）模型，观察ＴＰＮ过程中表皮生长因子（ＥＧＦ）对小肠谷氨酰胺（Ｇｌｎ）摄取及肠道免疫功能的调节作用。结果显示，常规ＴＰＮ可导臻血浆及各组织中Ｇｌｎ明显下降，肠粘膜淋巴细胞ＩＬ－２活性明显下降，细菌易位增高；而在ＴＰＮ过程中加用ＥＧＦ可防止肠道Ｇｌｎ水平下降，提高肠道对Ｇｌｎ的摄取率，并可有效防止肠粘膜淋巴细胞ＩＬ－２活性的下降，减少细菌易位。提示ＥＧＦ具有防止ＴＰＮ后     

肠饲谷氨酰胺对烧伤后肠道粘膜结构的保护作用

本研究利用３０％贵州小型香猪烧伤后早期肠道营养模型，在早期肠道营养液中加入谷氨酰胺，观察其对烧伤后肠道粘膜结构的保护作用。结果显示，伤后１０ｄ，单纯早期肠道营养组动物空肠、回肠粘膜的ＤＮＡ、ＲＮＡ和蛋白质含量，以及粘膜厚度、绒毛高度和隐窝深度均明显降...     

不同质蛋白对运动大鼠蛋白质及能量代谢的影响

观察了三种不同质的动、植物蛋白质组成的含蛋白质１７％的饲料对运动大鼠蛋白质及能量代谢的影响。实验取雄性断轧幼鼠３２只，随机等分为Ａ、Ｂ、Ｃ、Ｄ四组。饲料中蛋白质组成：Ａ组为１００％麦蛋白；Ｂ组酪蛋白１０％，麦蛋白９０％；Ｃ及Ｄ组均为酪蛋白４０％，麦蛋白６０％。Ａ、Ｂ、Ｃ组为观察不同质蛋白质对运动大鼠蛋白质及能量代谢的影响，Ｄ组为Ｃ组的安静对照组。观察指杯有体重、氮平衡、骨骼肌氮、血清尿素氮、血糖、血乳酸、肌糖元、肌轧酸脱氢酶、肌ＡＴＰ和肌Ｃａ２＋－ＡＴＰ酶活性。结果表明：１．不同质蛋白影响大鼠蛋白质代谢。Ａ组蛋白质最差、运动后大鼠呈负氮平衡，且血清尿素氮含量较高，肌氮较低，表明蛋白质分解代谢增强。２．不同质蛋白也影响大鼠能量代谢，Ｃ组蛋白质较好，运动时消耗了较多的肌糖原，产生较多的ＡＴＰ；ＬＤＨ和Ｃａ２－ＡＴＰ酶活性较高。３．相同质蛋白的Ｃ、Ｄ组，运动的Ｃ组在能量的产生及酶活性等方面，其数值稍高于安静对照的Ｄ组。４．从蛋白质及能量代谢看，以酪蛋白与麦蛋白４：６为适宜。     

富含谷氨酰胺和支链氨基酸经肠营养制剂效用的研究

在国产１７种氨基酸（１７ＡＡ）注射液组成的基础上，将支链氨基酸（ＢＣＡＡ）从１０．４％提高到３０．０％，同时增加１２．０％的谷氨酰胺（ＧＬＮ），调整其余氨基酸的含量，组成Ⅰ和Ⅱ配方。２１只Ｗｉｓｔａｒ雄性大鼠随机分成对照组、Ⅰ和Ⅱ组，每组７只，行创伤手术后，分别饲以Ⅰ、Ⅱ和对照组配方为氮源的合成饲料，各组饲料等氮、等能量。实验期为１４ｄ，通过测定创伤后大鼠的体重恢复、伤口愈合状况、尾血淋巴细胞转化反应及小肠粘膜中核酸和蛋白质含量等指标，比较两种处方对创伤大鼠恢复的效果。结果表明：富含ＢＣＡＡ、ＧＬＮ的配方Ⅰ和Ⅱ对创伤大鼠营养支持效果截然不同，其中Ⅰ组动物体重增长、前白蛋白恢复、淋巴细胞转化反应、小肠粘膜核酸及蛋白质含量、伤口皮肤抗张力强度及胶原蛋白合成量等指标均明显不如Ⅱ组及对照组（Ｐ＜０．０５）；反之，Ⅱ组动物的小肠粘膜核酸及蛋白质含量显著高于对照组和Ⅰ组（Ｐ＜０．０５），伤口皮肤抗张力强度及胶原蛋白合成量亦显著高于对照组和Ⅰ组（Ｐ＜０．０５）。提示：研制复合氨基酸配方除需考虑一些氨基酸的药理学作用外，还必须照顾各氨基酸的合理比例。     

Ala-Gln增强机体在全胃肠外营养状态下对失血性休克的耐受性

采用ＳＰＦ大鼠全胃肠外营养（ＴＰＮ）支持和失血性休克创伤模型，以ＴＰＮ、ＴＰＮ液中添加丙氨酰谷氨酰胺（Ａｌａ┐Ｇｌｎ）和经肠饮食（ＥＮ）三种营养方式支持一周后，造成失血性休克，观察机体因营养方式差异而处于不同肠屏障功能状态下对再次打击的耐受性。结果显示，标准ＴＰＮ组与ＥＮ相比，血浆二胺氧化酶（ＤＡＯ）水平明显低下；肠固有层（ＬＰ）淋巴细胞和浆细胞、肠上皮内淋巴细胞（ＩＥＬ）及肠腔细菌分泌型ＩｇＡ（Ｓ┐ＩｇＡ）包被率明显下降；盲肠粘膜菌群Ｅ．ｃｏｌｉ优势增殖，双歧杆菌／大肠杆菌（Ｂ／Ｅ）比值倒置，肠上皮细菌粘附增多；肠道细菌易位率升高；死亡率（４／１２）高。而Ａｌａ┐Ｇｌｎ组因添加肠道必需氨基酸谷氨酰胺（Ｇｌｎ）前体Ａｌａ┐Ｇｌｎ，各参数接近ＥＮ组，肠屏障储备增加，死亡率下降。提示：标准ＴＰＮ由于缺乏肠粘膜必需氨基酸（Ｇｌｎ）和肠道刺激，严重损伤肠屏障功能，失血性休克更加重损害，可能促发脓毒血症和多器官功能不全（ＭＯＤＳ）。对标准ＴＰＮ进行改良，添加肠粘膜保护剂Ａｌａ┐Ｇｌｎ对肠屏障有较好维持作用。这对临床不能经肠道喂养的围手术期病人进行如何更有效的肠外营养支持有一定指导意义     

^99mTc—DTPA测定肠道通透性的方法及应用

目的：建立９９ｍ锝┐乙三胺五乙酸（９９ｍＴｃ┐ＤＴＰＡ）测定肠道通透性的方法并观察其在临床和动物实验研究中的应用效果。方法：口服９９ｍＴｃ┐ＤＴＰＡ３７～７４ＭＢｑ，收集２４ｈ尿液，γ计数器测定尿液中ＤＴＰＡ排泄量。采用此方法观察了９例健康人和２５例胃肠道手术病人手术前及术后７天肠道通透性，３组病人术后７天分别给予谷氨酰胺０ｇ／（ｋｇ·ｄ）（Ａ组，ｎ＝８），０．３ｇ／（ｋｇ·ｄ）（Ｂ组，ｎ＝８）和０．６ｇ／（ｋｇ·ｄ）（Ｃ组，ｎ＝９）；１０头杂交猪自体小肠移植后分别给予标准全肠外营养（ＳＴＰＮ组，ｎ＝５）和强化３％甘氨酰谷氨酰胺的全肠外营养（ＧＴＰＮ组，ｎ＝５）２８天观察移植小肠的通透性。结果：９例健康人２４ｈ尿液ＤＴＰＡ排泄率为４．８６±１．８６％，术后７天Ａ、Ｂ二组病人ＤＴＰＡ排泄率较术前明显增加（６．６４±３．９５％ｖｓ１３．７１±４．８５％；８．８８±３．９５％ｖｓ１０．７６±２．８８％，Ｐ＜０．０５），Ｃ组手术前后肠道通透性无变化（６．８０±２．１２％ｖｓ３．５５±１．２９％，Ｐ＞０．０５）。术后２８天ＳＴＰＮ组ＤＴＰＡ排泄率明显高于ＧＴＰＮ组（２４．０１±７．４４％ｖｓ７．７７±３．０４％，Ｐ＜     

甘氨酰谷氨酰胺二肽改善猪自体移植小肠的吸收功能

目的：观察甘氨酰谷氨酰胺二肽对猪自体移植小肠吸收功能的作用。方法：杂种猪１０只,行自体小肠移植,术后随机分为两组,标准ＴＰＮ组（ＳＴＰＮ组,ｎ＝５）,接受标准ＴＰＮ支持８天;Ｇｌｙ－Ｇｌｎ二肽组（ＧＴＰＮ组,ｎ＝５）,接受含Ｇｌｙ－Ｇｌｎ的ＴＰＮ支持８天,术后１天（ＰＯＤ１）及术后２８天（ＰＯＤ２８）行木糖吸收实验,测定肠粘膜酶活性。结果：术后２８天,ＧＴＰＮ组：木糖吸收曲线下面积,５ｈ尿液木糖排     

Intact protein versus free amino acids in the nutritional support of thermally injured animals

This study compared the nutritional effects of intact protein with that of constituent amino acids as the sole source of nitrogen in a burn guinea pig model. Forty-five guinea pigs bearing a gastrostomy feeding tube were given 30% total body surface area, full thickness flame burn and were randomized into four groups. Group I (n = 12) and group III (n = 15) received a diet containing whey protein, while group II (n = 9) and group IV (n = 9) received an otherwise identical diet containing free amino acids in a whey protein pattern. Full strength continuous intragastric feeding was initiated immediately postburn in groups I and II, but a 72-hr adaptive period was provided in groups III and IV. Resting metabolic expenditure was measured by indirect calorimetry on postburn days 2, 6,9, and 13. After 14 days of enteral feeding, the animals were killed. Immediate enteral feeding of intact protein or free amino acids reduced postburn hypermetabolic response (p less than 0.01). However, the intact protein was found to maintain body weight and provide nitrogen retention better than the amino acid mixture (p less than 0.05). The animals on the intact protein diet also showed statistically significant benefits in carcass, liver, and gastrocnemius muscle weights and in serum albumin, transferrin and C3 levels. It is concluded that intact protein is superior to free amino acids for nutritional support following burn injury.     

The effect of route of nutrient administration on the nutritional state, catabolic hormone secretion, and gut mucosal integrity after burn injury

So that the efficacy of route of nutrient administration in thermal injury could be determined, a comparison was made between immediate enteral vs parenteral feedings in burned guinea pigs. Thirty-five guinea pigs underwent both catheter gastrostomy and jugular vein catheterization. On postoperative day 8, burned animals [30% total body surface area (TBSA)] were divided into an intragastrically (ig) fed group (N = 14) and a parenterally (iv) fed group (N = 14). Animals in each group received 175 kcal/kg/day with a solution of identical nutrient value beginning 2 hr after burn. The body weight change until postburn day (PBD) 8 and the average nitrogen balance were significantly better in the ig group than in the iv group. Values were also higher for the iv group than for the ig group in the early postburn period for urinary vanillyl mandelic acid (VMA) (p less than 0.05), plasma cortisol (p less than 0.05), and plasma glucagon (p less than 0.05). Also, the iv group showed reduced mucosal weight and thickness compared to the ig group on PBD 1 (p less than 0.02). There were significant negative correlations between VMA excretion and body weight change, and between plasma cortisol and jejunal mucosal structure (thickness and weight). These findings suggest that immediate postburn enteral nutrition can provide better nutritional support than parenteral nutrition through the maintenance of gut mucosal integrity and the prevention of increased secretion of catabolic hormones.     

The dipeptide alanyl-glutamine prevents intestinal mucosal atrophy in parenterally fed rats.

This study was performed to determine whether the addition of alanyl-glutamine (Ala-Gln) can prevent intestinal mucosal atrophy induced by standard solution of total parenteral nutrition (S-TPN). Forty-one male Sprague-Dawley rats weighing 250 g were randomly divided into four groups: group I was killed after overnight fasting; group II received S-TPN. The other groups received S-TPN supplemented with amino acids other than glutamine (group III) or supplemented with Ala-Gln 2 g/100 mL (group IV); both solutions were isocaloric and isonitrogenous. After 1 week of TPN the rats were killed, and the duodenum, proximal jejunum, mid-small bowel, and distal ileum were obtained for morphologic and functional analysis. Weight gain did not differ significantly among these four groups, and there was no difference in nitrogen balance between groups III and IV. Serum glutamine in group IV (102.8 +/- 13.3 mumol/dL) was significantly increased (p less than .05) compared with groups I, II, and III (66.2 +/- 3.9, 55.7 +/- 7.8, and 61.3 +/- 10.8 mumol/dL, respectively). Mucosal wet weight, protein, RNA, sucrase, and maltase of group IV were significantly increased (p less than .05) compared with groups II and III. Villus height was significantly increased (p less than .05) in the jejunum of group IV rats compared with groups II and III, but not in any other segments of the intestine. No significant changes were observed in crypt depth among all groups. Diamine oxidase in groups II, III, and IV was significantly decreased (p less than .05) compared with group I in all segments except for the ileum.(ABSTRACT TRUNCATED AT 250 WORDS)     

严重烧伤患者血清可溶性白介素-2受体含量变化及高压氧治疗对其影响

目的：本实验通过观察ＨＢＯＴ对烧伤患者血清可溶性白介素２受体（ｓＩＬ－２Ｒ）含量的影响，探讨其防治烧伤感染的意义。方法：选择烧伤总面积大于３０％或Ⅲ度面积大于１０％的烧伤患者４２例，随机分为高压氧治疗组和非高压氧组，８个时相点抽取静脉血，以ＥＬＩＳＡ法测定其血清ｓＩＬ－２Ｒ含量，同时比较两组患者脓毒症发生率。结果：非ＨＢＯＴ组患者伤后各时相点血清ｓＩＬ－２Ｒ含量显著高于正常；与此相反，ＨＢＯＴ组伤后各时相点血清ｓＩＬ－２Ｒ水平接近正常值，与非ＨＢＯＴ组相比，各时相点血清ｓＩＬ－２Ｒ水平显著降低，与此同时，脓毒症发生率也明显低于非ＨＢＯＴ组。结论：ＨＢＯＴ可显著降低烧伤患者血清ｓＩＬ－２Ｒ含量，故对防治烧伤感染可能有益。     

含合生元的早期肠内营养对严重烧伤病人血浆内毒素的影响

目的:探讨含合生元的早期肠内营养对严重烧伤病人血浆内毒素血症的影响。方法:随机双盲对照临床研究。40例重度烧伤病人分成含合生元(乳酸菌+纤维素)的早期肠内营养组(治疗组)和仅含纤维素的早期肠内营养组(对照组)。治疗前、伤后D3、D7、D10、D14和D21动态测定血内毒素水平。结果:几乎所有时相点治疗组血浆内毒素水平低于对照组,伤后D10有明显差异(P<0.05)且整个研究过程中治疗组内毒素血症发生率明显低于对照组(36.7%vs49.2%,P<0.05)。治疗组感染并发症较对照组也有所下降。结论:含合生元的早期肠内营养可以改善中毒以上烧伤病人内毒素血症的严重程度,对感染并发症产生了积极的影响。     

烧伤后维生素E的变化及其与脂质过氧化作用的关系

成年大鼠在体表面积15％Ⅲ度烧伤后,血清维生素E含量自烧伤后1.5小时至7天一直降低,以后逐渐回升,血清、肺组织中脂质过氧化物含量明显升高,3天后下降。血清超氧化物歧化酶和全血谷胱甘肽过氧化物酶活性均下降,前者在14天内不能恢复,后者在烧伤7天后逐渐恢复。烧伤大鼠经腹腔注射维生素E(20mg/100g体重),能明显抑制脂质过氧化物升高,血清、肺的抑制率分别为28％和31％。电镜观察:维生素E组大鼠肺组织未见损害改变,而对照组损害明显。结果表明:烧伤后及早补充维生素E是必要而有效的。     

Arginine-deficient diets alter plasma and tissue amino acids in young and aged rats.

Blood and urine metabolites were measured in two experiments for young (2-mo-old) and aged (20-mo-old) male Sprague-Dawley rats fed arginine-devoid diets made isonitrogenous to a control 1.12% arginine diet by adding alanine or glycine. Diet, fed for 7 or 13 d, had little effect on urinary or plasma ammonia and urea. Urinary orotate excretion was more than 40-fold higher in rats fed the arginine-deficient diets (P less than 0.01) in both experiments. Source of nonessential N (alanine or glycine) in the arginine-deficient diets did not alter orotic acid excretion or plasma or urine ammonia or urea. Changes in plasma arginine, alanine and glycine concentrations reflected the levels of these amino acids in the diet. Tissue ornithine levels reflected dietary arginine level, but tissue citrulline was unaffected by dietary arginine. Glutamate and glutamine were greater in the plasma and liver of rats fed arginine-deficient diets. Plasma concentrations of glutamate and glutamine were positively correlated with urinary orotic acid excretion (P less than 0.05) and ornithine and arginine were negatively correlated with orotic acid excretion (P less than 0.01). Increased tissue glutamine may be related to the greater orotate excretion in rats fed arginine-devoid diets. The metabolic responses to dietary arginine deficiency were similar in young and aged rats. In general, concentrations of amino acids in plasma, liver and spleen were higher in aged rats.     

Effects of nutrition on plasma, liver and muscle amino acids in scalded rats

This study set out to investigate the effect of three different parenterally administered diets on the free amino acid (AA) levels in the plasma, muscle, and liver of scalded rats. Diet I consisted of AA (1.4 g/100 g weight) and a high glucose dose (6 g/100 g weight), diet II consisted of AA and a low glucose dose (1.4 g/100 g weight) and in diet III only a low glucose dose was infused. Parenteral nutrition was started on the 3rd day posttraumatically. Sampling was performed on the 7th day posttraumatically. Nitrogen balances were significantly different in all three groups, being lowest in group III. Scalded rats fed isonitrogenously, but with different amounts of glucose showed only minor changes in AA concentrations. However scalded rats fed with a nitrogen-free diet exhibited significantly reduced total muscle and liver AA levels. These decreased AA levels were due to a drop of glycine in the muscle tissue (74%) and liver (49%). Contrary to the clinical catabolic situation in scalded and starved rats, it was not intracellular glutamine but glycine which was considerably influenced by catabolism and starvation.     

The effect of choline supplementation on hepatic steatosis in the parenterally fed rat

Information regarding hepatic function during total parenteral nutrition in rats is often extrapolated to the clinical situation, but the steatosis observed in that species may simply reflect choline deficiency and be irrelevant to man. The effect of choline supplementation on hepatic lipid content and triglyceride secretion was examined in parenterally fed rats. Eighty to 90-day-old rats were randomized into three groups; group I received oral Purina Chow ad libitum, groups II and III received identical total parenteral nutrition regimens with the exception that group III received supplemental choline. After 7 days, peripheral triglyceride uptake was inhibited with Triton WR1339, the rate of secretion of 14C-labeled triglyceride measured after a bolus injection of 1-14C-palmitic acid, and total hepatic lipid content was measured. Total hepatic lipid content was elevated in group II (86.3 mg/g) and group III (83.3 mg/g), and both differed significantly from the control group I (35.2 mg/g, p less than 0.01), but the choline supplementation appeared to make no difference. Hepatic secretion of 14C-palmitic acid as 14C-triglyceride was reduced in group II (0.73%/ml plasma), and group III (0.72%/ml plasma) compared to group I (1.06%/ml plasma, p less than 0.05), and was unaffected by choline. The hepatic steatosis produced in the parenterally fed rat did not appear to be due to choline deficiency but to some other factors which may be important in man.