术前全肠外营养与肠内联合肠外营养对克罗恩病手术治疗效果影响的比较分析

目的 评估术前采用全肠外营养(TPN)与肠内联合肠外营养(EN+PN)进行营养预康复对克罗恩病(CD)合并肠梗阻或肠瘘病人手术效果的影响。方法 回顾性分析2012-12-01—2021-12-01在南京大学医学院附属金陵医院普通外科炎症性肠病治疗中心因CD合并肠梗阻或肠瘘需要采用TPN或EN+PN进行营养预康复后行手术治疗的200例病人临床资料。根据采用营养预康复方式不同分为TPN组(137例)和EN+PN组(63例)。采用倾向性评分匹配(PSM)方法比较TPN组与EN+PN组营养治疗效果与术后30 d并发症的发生率。结果 PSM前,经营养预康复治疗后,TPN组和EN+PN组病人白蛋白水平和血红蛋白水平均较营养预康复治疗前升高,EN+PN组的白蛋白水平高于TPN组[(35.7±4.4)g/L vs.(33.5±5.4)g/L,t=-2.79,P=0.003];EN+PN组C-反应蛋白低于TPN组,但差异无统计学意义[6.3(1.1,20.5)mg/Lvs.9.9(2.3,30.0)mg/L,Z=-1.27,P=0.201];EN+PN组血红蛋白水平高于TPN组(112.5±15.5 g...     

乌司他丁和全肠外营养对胃肠道恶性肿瘤患者术后急性相蛋白代谢的影响

目的探讨乌司他丁 (UTI)和全肠外营养 (TPN)对胃肠道恶性肿瘤患者术后急性相蛋白代谢的影响。方法 6 0例胃肠道恶性肿瘤患者行根治性切除术后 ,随机分为对照组、UTI组、TPN组和UTI+TPN组 ,每组各 15例。结果急性相蛋白于术后 3d ,对照组、TPN组显著低于其余两组 (P <0 0 1) ;术后 7d ,UTI+TPN组显著高于其余组 (P <0 0 1)。术后 4d起UTI+TPN组已接近正氮平衡 ,与其余组比较 ,差异有显著性意义 (P <0 0 1)。结论胃肠道恶性肿瘤患者术后应用UTI和TPN可促进急性相蛋白合成 ,减少净蛋白丢失 ,有利于机体顺利度过应激反应期。     

联合应用生长激素和谷氨酰胺对短肠大鼠小肠粘膜上皮细胞基因表达的影响

目的　探讨联合应用生长激素和谷氨酰胺防止小肠粘膜萎缩的分子学机制。方法　选用 40只手术成功的SD短肠大鼠 ,随机均分为 4组 ,分别给予常规全肠外营养 (TPN组 )、附加谷氨酰胺 (TPN +Gln组 )、附加生长激素 (TPN +GH组 )及附加谷氨酰胺和生长激素全肠外营养(TPN +GH +Gln组 ) ,持续 6d。另取 8只正常大鼠模拟手术后第 1天处死 ,作为基础对照组 (Con trol组 )。应用逆转录 聚合酶链式反应 (RT PCR)技术检测残留小肠粘膜上皮细胞c fos和c junmRNA的表达。结果　小肠粘膜上皮细胞c fos和c junmRNA表达值中 ,TPN组 (0 .1 1± 0 .0 7、0 .2 9± 0 .1 0 )明显低于对照组 (0 .48± 0 .1 5、0 .57± 0 .2 2 ,P <0 .0 5) ;TPN +Gln和TPN +GH组 (分别为 0 .32± 0 .1 5和 0 .48± 0 .2 1 ,0 .36± 0 .1 3和 0 .46± 0 .1 7) ,较TPN组显著增高 (P <0 .0 5) ;TPN +GH +Gln组 (0 .35± 0 .1 6、0 .61± 0 .1 3)明显高于TPN组 (P <0 .0 5) ,与对照组差异无显著性。结论　生长激素或谷氨酰胺单独应用均可通过上调小肠粘膜上皮细胞c fos和c jun基因的表达 ,促进细胞分裂增殖 ,从而防止小肠粘膜萎缩的发生 ,且两者联合应用具有协同增效作用     

谷氨酰胺添加剂对腹腔镜Miles手术后营养及T细胞的影响

研究早期肠内营养(EEN)添加谷氨酰胺对腹腔镜Mile s手术后营养及T细胞的影响。将腹腔镜Mile s手术患者分为全肠外营养(TPN)治疗组(TPN组)、EEN治疗组(EEN组)和EEN添加谷氨酰胺治疗组(GEN组),比较3组患者手术前后营养指标(PA、ALB和TP)和T细胞免疫(CD3~+、CD4~+和CD8~+)的差异。TPN组、EEN组和GEN组患者手术前1 d的PA、ALB、TP、CD3~+、CD4~+和CD8~+差异均无统计学意义(P0.05),手术后7 d的PA、ALB、TP、CD3~+、CD4~+和CD8~+较手术前均显著增加(P0.05);GEN组患者手术后7 d的PA、ALB、TP、CD3~+、CD4~+和CD8~+均显著高于TPN组和EEN组患者(均P0.05)。EEN添加谷氨酰胺可显著改善直肠癌腹腔镜Mile s手术后患者的营养及T细胞免疫,其疗效显著高于EEN和TPN。     

一氧化氮对正常及肝硬化大鼠全胃肠外营养肝损害的影响

目的　探讨一氧化氮（Nitricoxide,NO）在全胃肠外营养(Total Parenteral Nutrition,TPN)导致正常肝脏及肝硬化大鼠肝损害中的影响。　方法　30只正常Wistar大鼠和30只肝硬化Wistar大鼠各自分别随机分为5组A组,自由进食和水;B组,TPN;C组,TPN+精氨酸;D组TPN+N     

重症急性胰腺炎肠外、肠内营养的分期应用

目的 探讨重症急性胰腺炎(SAP)手术后早期应用肠内营养的可行性并比较肠内营养(EN)与肠外营养(PN)的效果。方法 本组将16例患者分为完全胃肠外营养(TPN)组和PN+EN组,每组各8例。TPN组患者于术后第2天开始TPN支持,大部分为7～10 d,其中1例最长达64 d。EN组行TPN支持7～10 d后逐渐过渡至PN+EN,再过渡至EN或口服饮食。结果 两组术后体重及白蛋白较术前明显降低(P<0.01),但组间比较无统计学意义。肝功能变化:手术前后两组ATL、AST、AKP、GGT组间比较无明显差异(P>0.05),组内比较PN+EN组术后ALT、AST均有不同程度增高。两组术后GGT均高于手术前(P<0.01),TPN组术后增高更明显。PN+EN组手术前后AKP变化无统计学意义(P>0.05);但TPN组术后AKP高于术前且有统计学差异(P<0.05)。TPN组LDH术后高于PN+EN组(P<0.05),两组TBIL营养支持前后比较无统计学意义。结论 ①患者的高分解代谢并不因外源性营养底物而逆转。②两种支持方式术后短期应用总体疗效差异不明显,长期应用PN+EN优于TPN。③与TPN相比,EN具有符合生理、安全、有效、价廉等优点。     

肠内及全肠外营养支持对恶性胸水患者免疫功能的影响

目的 比较肠内(EN)与全肠外营养(TPN)支持对恶性胸水患者机体免疫功能的影响,探讨恶性胸水患者合理的营养支持方式.方法 采用前瞻性对比研究,将45例恶性胸水患者随机分为EN组和TPN组,分别给予EN和TPN支持治疗.于治疗开始之前检查所有患者的外周血IgA、IgG、IgM、淋巴细胞总数(TLC)及T 细胞亚群CD3+、CD4+百分率和CD4+/CD8+比值 ,于治疗两周后复查上述指标.结果 EN组IgG、TLC、CD4+T细胞以及CD4+/CD8+比值在营养支持前后及与TPN组相比获得明显改善(P<0.05).结论 EN支持可提高恶性胸水患者机体免疫功能,效果优于TPN支持.     

重症急性胰腺炎完全胃肠外营养与肠外联合肠内营养治疗对比研究

目的 观察重症急性胰腺炎(SAP)完全胃肠外营养(TPN)与肠外营养(PN)联合肠内营养(EN)治疗中各项指标的变化,分析二者疗效.方法 29例SAP随机分为TPN组(14例)和PN+EN组(15例),并均行非手术治疗14 d,观察疗效及化验指标的变化.结果 营养支持治疗14 d后,各组血清白蛋白(ALB)、总蛋白(TSP)、血钙(Ca2+)、谷丙转氨酶(ALT)、谷草转氨酶(AST) 较营养支持前均显著升高(P<0.05);各组血糖、血清淀粉酶、血WBC均较营养支持前显著下降(P<0.05);各组血总胆红素(TB)治疗前后差异无统计学意义(P>0.05);PN+EN组血WBC显著低于TPN组(P<0.05),其余化验指标组间比较差异无统计学意义(P>0.05);各组APACHEⅡ评分较治疗前显著降低(P<0.05),PN+EN组评分显著低于TPN组(P<0.05).PN+EN组住院天数、住院总费用、感染发生率及死亡率均显著低于TPN组(P<0.05).结论 PN联合EN治疗SAP优于TPN.     

重症急性胰腺炎完全胃肠外营养与肠外联合肠内营养治疗对比研究

目的 观察重症急性胰腺炎(SAP)完全胃肠外营养(TPN)与肠外营养(PN)联合肠内营养(EN)治疗中各项指标的变化,分析二者疗效.方法 29例SAP随机分为TPN组(14例)和PN+EN组(15例),并均行非手术治疗14 d,观察疗效及化验指标的变化.结果 营养支持治疗14 d后,各组血清白蛋白(ALB)、总蛋白(TSP)、血钙(Ca2+)、谷丙转氨酶(ALT)、谷草转氨酶(AST) 较营养支持前均显著升高(P<0.05);各组血糖、血清淀粉酶、血WBC均较营养支持前显著下降(P<0.05);各组血总胆红素(TB)治疗前后差异无统计学意义(P>0.05);PN+EN组血WBC显著低于TPN组(P<0.05),其余化验指标组间比较差异无统计学意义(P>0.05);各组APACHEⅡ评分较治疗前显著降低(P<0.05),PN+EN组评分显著低于TPN组(P<0.05).PN+EN组住院天数、住院总费用、感染发生率及死亡率均显著低于TPN组(P<0.05).结论 PN联合EN治疗SAP优于TPN.     

重症急性胰腺炎早期应用肠内营养临床疗效分析

目的观察重症急性胰腺炎(SAP)患者早期肠内营养(EEN)治疗的疗效。方法将65例SAP患者随机分成EEN组(33例)和TPN组(32例)。EEN组患者采取早期EEN+TPN治疗,并逐渐减少TPN的用量,直至停止TPN;TPN组患者采取TPN治疗。观察2组患者腹痛的缓解时间、住院期间花去的费用、住院的天数以及是否出现并发症。结果:2组患者通过营养支持后EEN组的腹痛缓解时间、住院时间、花去费用以及并发症发生率均低于TPN组(P0.05)差异具有统计学意义。结论 EEN治疗可显著提高SAP患者的治愈率,降低感染率及并发症的发生,并缩短住院时间。     

精氨酸对肝硬化肝癌患者术后全胃肠外营养的肝脏保护作用

目的 研究精氨酸对原发性肝癌（primary liver cancer,PLC)伴肝硬化病人术后全胃肠外营养（total parenteral nutrition,TPN)时的肝脏保护作用。方法 将30例行肝段或肝叶切除手术的病人随机分为对照组（TPN组）及实验组（TPN＋精氨酸组）。观察病人术前、术后1d及7d肝功能、血脂、免疫功能及血清一氧化氮（nitric oxide,NO)浓度变化,并在术中及术后7d取肝组织作病理学检查。结果 与对照组比较,实验组术后7d AST、TBIL已接近术前水平,ALB明显降低,TG仍比术前低,CD4^ 水平和NO浓度升高,肝脂肪变性程度下降。结论 补充精氨酸可增加NO浓度,减轻TPN时的肝脂肪沉积程度,降低血脂水平,加快术后肝酶活性恢复,改善和提高肝癌病人术后细胞免疫功能。     

肉毒碱治疗TPN大鼠肝脂肪变性的研究

目的 探讨在全胃肠外营养（ＴＰＮ）中补充肉毒碱减轻肝脂肪变性的作用。方法 １８只正常Ｗｉｓｔａｒ大鼠和１９只肝硬化Ｗｉｓｔａｒ大鼠分别随机分为６组,Ａ１组、Ａ２组,自由进食和进水（各６只）;Ｂ１组、Ｂ２组,ＴＰＮ（分别６只、７只）;Ｃ１组、 ,ＴＰＮ加肉毒碱（各６只）。各组实验结束后测肝功能,肝脂肪及行肝脏的组织学检查。结果 ＴＰＮ组肝内脂肪显著２,ＴＰＮ＋肉毒碱组肝内脂肪明显减少。结论 在ＴＰＮ     

Addition of L-glutamine to total parenteral nutrition and its effects on portal insulin and glucagon and the development of hepatic steatosis in rats

Infusion of total parenteral nutrition (TPN) with excess carbohydrate calories leads to hepatic steatosis in rats and is associated with an elevated portal insulin/glucagon molar ratio. Previously we have shown that adding glucagon to TPN prevents and reverses hepatic steatosis in rats, possibly by increasing hepatic lipid export. It has been reported that steatosis is eliminated in rats by the addition of L-glutamine to TPN. In this study, we examined the effect of glutamine on portal insulin and glucagon levels and the development of hepatic steatosis. Adult rats (n = 19) received internal jugular catheters: Group 1 (n = 6), saline (3 cc/hr) and chow ad libitum; Group 2 (n = 7), 25% dextrose base TPN; Group 3 (n = 6), 25% dextrose base TPN with 2% glutamine. The infusion rate of TPN was 1.2 cc/100 g body wt/hr. Daily nitrogen balance was determined and at 7 days, portal venous blood was drawn for insulin and glucagon radioimmunoassay, livers were removed for histology and lipid content determination, and the small intestines were removed for mucosal protein and DNA content determination. Panlobular vacuolization of the hepatocytes was noted on histology in Group 2 (TPN) while Group 1 (chow) and Group 3 (TPN + glutamine) showed normal liver morphology. Hepatic lipid content was significantly elevated in Group 2 (P less than 0.05). The portal insulin/glucagon molar ratio was increased because of excessive portal venous insulin in Group 2 (TPN). In contrast, portal glucagon was significantly elevated while the insulin/glucagon ratio and hepatic lipid content did not increase above control levels in the glutamine-supplemented Group 3 rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

一氧化氮对急性胆道感染大鼠肾功能影响作用研究

目的　探讨一氧化氮（nitric oxide,NO）对实验性急性胆道感染大鼠肾功能的影响作用。方法　Wistar大鼠35只,随机分为急性胆道感染组（AC组）、急性胆道感染加左旋精氨酸组（L组）、左旋硝基精氨酸甲基酯组（N组）、单纯胆道梗阻对照组（O组）和假手术组（SO组）5组,分别测定血浆NO、BUN、Cr值和肾组织一氧化氮合成酶（NOS）活性,并行肝、肾组织病理变化观察。结果　L组NO、NOS高于其余各组（P＜0.05）,BUN、Cr低于AC组和N组（P＜0.05）,而与O组比较差异无显著性意义（P＞0.05）,肾组织病理变化较AC组轻;N组NO、NOS低于其余各组,而BUN、Cr则高于其余各组（P＜0.05）。结论　NO对急性胆道感染72小时大鼠的肾功能有保护作用,其作用机理可能与其舒张肾血管,增加血液灌流量等作用有关。     

Reversal of hepatic steatosis in rats by addition of glucagon to total parenteral nutrition (TPN)

Infusion of total parenteral nutrition (TPN) with excess carbohydrate calories leads to hepatic steatosis in rats that is associated with an elevated portal insulin/glucagon molar ratio. Previously we have shown that adding glucagon to TPN prevents hepatic steatosis in rats. In this study we attempted to reverse the steatosis by adding glucagon to TPN after 1 week of TPN alone. Adult rats (n = 28) received internal jugular catheters: Group 1 (n = 7), saline (3 cc/h) and chow ad libitum; Group 2 (n = 7), 25% dextrose base TPN solution for 1 week; Group 3 (n = 7), 25% dextrose base TPN for 2 weeks; Group 4 (n = 7), 25% dextrose base TPN for 1 week and then glucagon (15 micrograms/100 g/day) added to TPN for the second week. The infusion rate of TPN was 1.2 ml/100 g/hr (40% kcal greater than control). At 7 days (Group 2) and 14 days (Groups 1, 3, and 4) portal and peripheral venous blood levels were drawn for insulin and glucagon radioimmunoassay, blood glucose determination, and liver function tests; livers were removed for histology and lipid content determination. Blood glucose was equivalent among all groups. Liver function tests were within normal limits. Panlobular vacuolization of the hepatocytes was noted on histology in Groups 2 and 3. Hepatic lipid content was significantly elevated in Group 3. The portal insulin/glucagon molar ratio was increased because of excessive portal venous insulin in Groups 2 and 3 (P less than 0.05 by ANOVA). In contrast, portal venous insulin and the insulin/glucagon molar ratio did not increase in Group 4 and hepatic lipid infiltration was absent when glucagon was added to the TPN solution after 1 week of TPN solution alone. The results suggest that the addition of glucagon to hypertonic dextrose TPN is not only protective in preventing hepatic steatosis, but may reverse steatosis, possibly by increasing hepatic lipid export.     

Addition of glucagon to total parenteral nutrition (TPN) prevents hepatic steatosis in rats

Hepatic steatosis is one of the two principal hepatic complications of total parenteral nutrition (TPN), the other being cholestasis. While the cause is uncertain, an excess of carbohydrate calories in rats leads to an elevated portal insulin/glucagon (I/G) molar ratio, periportal fatty infiltration, and increased total hepatic lipid content. Insulin causes fatty acid biosynthesis, whereas glucagon causes hepatic release and inhibition of fatty acid synthesis. Thus we attempted to add glucagon to lower the I/G to see if this would affect the degree of hepatic fatty infiltration by encouraging hepatic fat mobilization. Adult rats (n = 21) received internal jugular catheters; Group 1 (n = 7) was given saline solution (3 ml/h) and chow ad libitum; Group 2 (n = 7), 25% dextrose-base (D25W) TPN solution; Group 3 (n = 7), D25W TPN + 33 micrograms/100 gm/day glucagon. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay and blood glucose determination; livers were removed for histologic study and lipid determination. Blood glucose did not differ in any group. Hepatic lipid and peripheral and portal venous I/G were increased and periportal fatty infiltration was extensive in Group 2, whereas hepatic lipid and I/G were decreased and periportal fatty infiltration was absent in glucagon-infused rats (Group 3). An abnormally high I/G ratio in portal blood elicited by high-glucose TPN may be responsible, at least in part, for hepatic steatosis. By increasing hepatic lipid export, addition of glucagon to TPN may play a major role in decreasing hepatic steatosis.     

戊四氮致痫大鼠海马一氧化氮的变化及对海马神经元凋亡的影响

目的 观察戊四氮(PTZ)致痫大鼠海马一氧化氮(NO)的变化对神经元兴奋毒性的影响.方法 SD雄性大鼠随机分为3组,每组14只,分别用生理盐水(A组)、PTZ(B组)、氨基胍+PTZ(C组)造模后,对海马NO含量、谷氨酸(Glu)免疫反应性、半胱氨酸酶(Caspase)-3 mRNA水平进行检测分析.结果 B组海马NO含量为(75.67±2.04) μmol/L,与A组(11.90±0.64) μmol/L和C组(36.19±4.48) μmol/L比较差异有统计学意义(P＜0.05);A组和C组的Glu、caspase-3 mRNA 表达水平明显低于B组(P＜0.05).结论 戊四氮致痫后可导致大鼠海马NO过量产生,对海马神经元具有兴奋毒性作用.而一氧化氮合成酶抑制剂的干预,具有神经保护作用.     

半肝入肝血流加肝静脉阻断在规则性肝切除术中的应用

目的：探讨半肝入肝血流加肝静脉阻断术在规则性肝切除术中的意义。方法：行半肝入肝血流加肝静脉阻断术42例（A组）、半肝入肝血流阻断术30例（B组）、全肝入肝血流阻断术30例（C组）,比较3组患者的手术时间、术中出血量以及术后第1、3、6天的血清谷丙转氨酶（ALT）、胆红素、白蛋白水平和术后并发症的发生率。结果：术中平均出血量分别为（453.5±87.9）、（612.8±101.6）和（646.7±136.6）mL,A组显著低于B组和C组（P〈0.05）,B组和C组间差异无统计学意义（P〉0.05）,3组患者的手术时间差异无统计学意义（P〉0.05）;A组和B组在术后第3、6天的血清ALT、胆红素水平显著低于C组,而血清白蛋白水平显著高于C组（P〈0.001）,A组和B组间差异无统计学意义（P〉0.05）;A组和B组的术后腹水发生率均显著低于C组（P〈0.01）。结论：半肝入肝血流加肝静脉阻断术可显著减少肝切除术中的出血,减轻术中、术后肝功能的损害,是一种安全、有效的肝切除方法。     

Hepatic steatosis due to total parenteral nutrition: the influence of short-gut syndrome, refeeding, and small bowel transplantation

This study was undertaken to determine whether refeeding through the native small intestine or through a small bowel transplant would reverse hepatic steatosis induced by total parenteral nutrition (TPN), and of what influence a coexisting short-gut syndrome is. Three short-gut syndromes of different severity were established in Lewis rats (short-gut I, mild; short-gut II, moderate; short-gut III, severe). TPN was administered for 10 days and the animals were refed for 20 days. A liver biopsy after the TPN period confirmed a mild to moderate fatty infiltration of the liver in all groups. After the refeeding period a second liver biopsy was obtained and no evidence of hepatic steatosis was observed in Groups 1, 2, 3, and 4 (normal Lewis rat, short-gut I, II, and III). The animals in group 5 (short-gut I) received a syngeneic small bowel transplant after discontinuation of TPN. After the refeeding period the liver biopsies showed no evidence of fatty infiltration. The intestinal graft also reversed the nutritional deficiencies which were observed in the animals with short-gut and showed normal body weight gain and nitrogen and fat uptake in comparison to the normal animals (Group 1). These data show that a small bowel graft is capable of reversing the deleterious sequelae of short-gut syndrome as well as the TPN-related hepatic steatosis.