早期肠内营养对急性重症胰腺炎大鼠肠道粘膜屏障的保护作用

目的 探讨早期肠内营养对急性重症胰腺炎大鼠肠道粘膜屏障的保护作用。方法 SD大鼠48只，随机分成6组（n=8)；急性重症胰腺炎全肠外营养1天组（A组），模拟手术全肠外营养1天组（B组），急性重症胰腺炎全肠外营养5天组（C组）和肠内营养5天组（E组），模拟手术全肠外营养5天组（D组）和肠内营养5天组（F组）。采用逆行胰胆管注射3%牛磺胆酸钠溶液制成重症胰腺炎大鼠模型。E组和F组术后先予肠外营养，48h后开始肠内营养，观察大鼠的空肠组织形态学变化及空肠粘膜固有层CD4^ /CD8^ 比值。结果 急性重症胰腺炎大鼠均无死亡，E组和F组大鼠对肠内营养耐受良好，C组的CD4^ /CD8^ 比值明显低于D组。E组的空肠绒毛高度和CD4^ /CD8^ 比值明显高于C组。结论 重症胰腺炎大鼠肠道粘膜屏障功能受损。早期肠内营养可改善重症胰腺炎大鼠的肠道粘膜屏障功能。     

鱼油对重症急性胰腺炎大鼠肠黏膜屏障的影响

目的:探讨 -3鱼油脂肪乳剂对重症急性胰腺炎(SAP)大鼠早期肠黏膜功能屏障的影响.方法:♂Wistar大鼠30只随机分为:假手术组(So组,n=10),鱼油治疗组(F组,n=10)和生理盐水治疗组(N组,n=10).通过胰管逆行注射法建成SAP模型,并分别尾静脉注射 -3鱼油脂肪乳剂和生理盐水治疗.检测大鼠血浆D-乳...     

复合乳酸菌对不同营养治疗途径的重症急性胰腺炎大鼠肠屏障功能的影响

目的:观察复合乳酸菌对早期肠内营养(EEN)和肠外营养(PN)治疗的重症急性胰腺炎(SAP)大鼠肠屏障功能的影响.方法:♂ SD大鼠胰腺被膜下均匀注射38 g/L牛磺胆酸钠制作SAP模型,96只大鼠随机分为假手术早期肠内营养治疗组(Sham-EEN)、早期肠内营养治疗组(EEN)、早期肠内营养联合复合乳酸菌治疗组(EEN Lac);假手术肠外营养治疗组(Sham-PN)、肠外营养治疗组(PN)、肠外营养联合复合乳酸菌组(PN Lac),每组16只,分别于第4和7天随机取8只大鼠,预处理后取材,检测肝和肠系膜淋巴结(MLN)肠道菌群易位(BT)、血浆内毒素(ET)、肠转运指数,TUNEL法检测肠上皮细胞凋亡、BCA法测定小肠黏膜蛋白含量、ELISA法测定小肠黏液SIgA含量.结果:PN组大鼠的BT率高于EEN组和PN Lac组(14/16 vs 9/16,10/16,均P＜0.05);4 d EEN组高于EEN Lac组(12/16 vs 9/16,P=0.026).PN组血浆ET高于EEN组(276.83±30.81 EU/Lvs 138.52±22.56 EU/L,P＜0.05);不加用Lac组高于加用Lac组(均P＜0.05).PN Lac组肠转运系数高于PN组(0.70±0.08 vs 0.59±0.05,P＜0.01).PN组小肠上皮细胞AI高于EEN组和PN Lac组(22.67%±4.97% vs 15.31%±4.18%,18.40%±2.01%,P＜0.01).加用Lac组空肠黏膜蛋白含量高于不加用Lac组(均P＜0.05);EEN Lac组高于PN Lac组(56.91±3.73 mg/gvs 44.69±2.99 mg/g,P＜0.01).EEN Lac组小肠黏液SIgA含量高于EEN组和PN Lac组(82.17±6.02 μg/g vs 69.26±5.66 μg/g,59.87±5.54μg/g,P＜0.05及P＜0.01).结论:加用复合乳酸菌可改善EEN和PN治疗的SAP大鼠肠屏障功能,其中EEN Lac的作用最为显著,EEN在维护SAP大鼠肠屏障方面的作用优于PN.     

重症急性胰腺炎肠屏障功能障碍研究

重症急性胰腺炎患者常伴有肠屏障功能障碍,正常肠道屏障由机械屏障、化学屏障、免疫屏障与微生物屏障4部分构成.肠屏障功能障碍通常指上述4种屏障功能出现不同程度的破坏,本文就重症急性胰腺炎肠道屏障功能障碍时上述4种屏障的病理生理改变作一概述.     

早期肠内营养联合肠屏障保护剂治疗急性重症胰腺炎64例

目的:探讨早期肠内营养联合肠屏障保护剂在急性重症胰腺炎治疗中的应用价值.方法:将64例SAP患者随机分三组,A组予常规治疗,B组在常规治疗基础上通过鼻空肠管给予早期肠内营养,C组通过鼻空肠管给予早期肠内营养并加用肠屏障保护剂.观察患者症状、体征、WBC、CRP、血淀粉酶恢复正常时间,其体质量及血清白蛋白变化情况以及对比其总住院费用、平均每天的住院费用及住院时间.结果:B组在症状、体症、WBC、CRP、血淀粉酶恢复时间以及住院时间、住院费用均明显优于A组(P<0.05).C组在CRP及白细胞数恢复时间上更是优于B组,但平均每天住院费用三组没有明显差异性(P>0.05).结论:在SAP治疗中应用鼻空肠管进行早期肠内营养联合肠屏障保护剂,可以改善SAP患者的营养状况,加快症状恢复,缩短病程,减少医疗费用.     

益生菌结合早期肠内营养对重症急性胰腺炎患者营养状况、肠黏膜屏障功能及肠内营养耐受性的影响

目的观察分析益生菌结合早期肠内营养对重症急性胰腺炎患者营养状况、肠黏膜屏障功能及肠内营养耐受性的影响。 方法选取2020年1月至2021年5月淮安市第二人民医院收治的92例重症急性胰腺炎患者,按照随机数字表法随机分为试验组与对照组,每组各46例。对照组患者采取早期肠内营养进行治疗,试验组施行益生菌结合早期肠内营养进行治疗。比较2组患者营养状况、肠黏膜屏障功能及肠内营养耐受性等主要指标。 结果治疗后,试验组血清白蛋白、前白蛋白、转铁蛋白、上臂肌围及肱三头肌皮褶厚度等营养指标的增加程度高于对照组,试验组乳杆菌、肠球菌及双歧杆菌等有益菌的总量高于对照组,试验组肠道黏膜屏障中的D-乳酸、二胺氧化酶含量及血浆内毒素水平低于对照组,差异均有统计学意义(P<0.05)。试验组患者肠道菌群和肠道黏膜屏障等指标的改进状况比对照组患者更理想。 结论益生菌结合早期肠内营养应用于重症急性胰腺炎患者可以达到良好的疗效。     

持续低效血液透析滤过对重症急性胰腺炎患者肠黏膜屏障功能及免疫功能的影响

目的 评价持续低效血液透析滤过（SLEDF）对重症急性胰腺炎（SAP）患者肠黏膜屏障功能及免疫功能的影响。方法 将51例SAP患者随机分为持续静脉静脉血液滤过（CVVH）组25例和SLEDF组26例,在常规治疗基础上分别接受CVVH和SLEDF治疗。比较两组患者预后、血、尿淀粉酶恢复正常时间、治疗前和治疗第2、4、8、14d血D-乳酸、内毒素（ET）、二胺氧化酶(DAO)、CD3⁺、CD4⁺、CD8⁺T淋巴细胞水平、CD4⁺/CD8⁺T淋巴细胞比值及血液净化相关并发症发生情况。结果 两组患者死亡率、血、尿淀粉酶恢复正常时间比较差异均无统计学意义,血D-乳酸、ET、DAO、CD3⁺、CD4⁺、CD8⁺T淋巴细胞水平和CD4⁺/CD8⁺T淋巴细胞比值在治疗前和治疗第2、4、8、14d比较差异均无统计学意义（P>0.05）。两组患者治疗第4、8、14d D 乳酸、ET和DAO水平均较同组治疗前降低,第8、14d均较同组治疗第4d降低（P＜0.05）。两组患者治疗第4、8、14d的CD3⁺、CD4⁺、CD8⁺T淋巴细胞水平和CD4⁺/CD8⁺T淋巴细胞比值均较同组治疗前升高,第8、14d均较同组治疗第4d升高（P＜0.05）;两组患者治疗第4、8d的CD8⁺T淋巴细胞水平较同组治疗前降低,第8、14d较第4d降低（P＜0.05）。结论 SLEDF和CVVH改善SAP患者肠道屏障功能障碍和免疫功能异常的作用相似,其中SLEDF操作方便,医疗费用低,值得临床推广。     

Role of gut microbiota on intestinal barrier function in acute pancreatitis

Acute pancreatitis(AP) is a common gastrointestinal disorder. Approximately15%-20% of patients develop severe AP. Systemic inflammatory response syndrome and multiple organ dysfunction syndrome may be caused by the massive release of inflammatory cytokines in the early stage of severe AP,followed by intestinal dysfunction and pancreatic necrosis in the later stage. A study showed that 59% of AP patients had associated intestinal barrier injury,with increased intestinal mucosal permeability, leading to intestinal bacterial translocation, pancreatic tissue necrosis and infection, and the occurrence of multiple organ dysfunction syndrome. However, the real effect of the gut microbiota and its metabolites on intestinal barrier function in AP remains unclear. This review summarizes the alterations in the intestinal flora and its metabolites during AP development and progression to unveil the mechanism of gut failure in AP.     

Acute pancreatitis is characterized by generalized intestinal barrier dysfunction in early stage

Background and aimsThe role of intestinal-barrier in acute pancreatitis(AP) is poorly understood. We aimed to assess structural and functional changes in the intestinal-barrier in patients with early AP (time from onset<2 weeks) and the effect of enteral nutrition on them.MethodsIn this prospective observational study, patients with early AP not on enteral nutrition were compared with controls for baseline intestinal-permeability(lactulose: mannitol ratio(L:M)), endotoxinemia(serum IgM/IgG anti-endotoxin antibodies), bacterial-translocation(serum bacterial 16S rRNA) and duodenal epithelial tight-junction structure by immunohistochemistry(IHC) for tight-junction proteins(claudin-2,-3,-4, zonula occludens-1(ZO1), junctional adhesion molecule(JAM) and occludin) and electron microscopy. These parameters were reassessed after 2 weeks enteral feeding in a AP patients subset.Results96 patients with AP(age: 38.0 ± 14.5 years; etiology: biliary[46.8%]/alcohol[39.6%]; severe:53.2%, mortality:11.4%) and 40 matched controls were recruited. Patients with AP had higher baseline intestinal permeability(median L:M 0.176(IQR 0.073–0.376) vs 0.049(0.024–0.075) in controls; p < 0.001) and more frequent bacteraemia(positive bacterial 16S rRNA in 24/48 AP vs 0/21 controls; p < 0.001) with trend towards higher serum endotoxinemia(median IgG anti-endotoxin 78(51.2–171.6) GMU/ml vs 51.2(26.16–79.2) in controls; p = 0.061). Claudin-2, claudin-3, ZO1 were downregulated in both duodenal crypts and villi while claudin-4 and JAM were downregulated in duodenal villi and crypts respectively. 22 AP patients reassessed after initiation of enteral nutrition showed trend towards improving intestinal permeability, serum endotoxinemia and bacteraemia, with significant improvement in claudin-2,-3 in duodenal villi.ConclusionPatients with AP have significant disturbances in intestinal barrier structure and function in first 2 weeks from onset that persist despite institution of enteral nutrition.     

添加益生元肠内营养对重症急性胰腺炎肠屏障损害和内毒素易位的作用

目的:研究重症急性胰腺炎(SAP)大鼠早期给予添加益生元的微生态肠内营养后对肠屏障损害和内毒素易位的作用及其机制.方法:根据SAP营养代谢特点配制专用EN配方(EN-S),并添加低聚半乳糖益生元制成微生态肠内营养配方(RPE-EN).64只SD大鼠被随机分成8组(n=8):假手术对照4d组,假手术对照7d组,SAP EN-S治疗4d组、SAP EN-S治疗7d组、SAP PRE-EN治疗4d组、SAP PRE.EN治疗7d组、SAP PN治疗4d组、SAP PN治疗7d组.采用胰被膜下均匀注射38g/L牛磺胆酸钠法建立SAP大鼠模型,营养治疗在模型建立成功后即开始.分别在第4天和第7天处死大鼠,分别采用偶氮基质显色法和辣根过氧化物酶检测血浆内毒素和二胺氧化酶(DAO)水平,采用TUNEL法检测小肠上皮细胞凋亡,并计算凋亡指数(AI).结果:EN-S、PRE-EN及PN组的血浆内毒素(4d组:158.7±23.9,110.4±14.4,202.0±30-3 EU/Lvs 39.6±13.1 EU/L:7d组:140.5±20.9.88.16±30.4.210.2±30-3 EU/Lvs 40.7±12.4 EU/L)、DAO(4d组:5.17±0.62,3.44±0.59.7.29±0.68 kU/Lvs 2.01±0-34 kU/L:7d组:4.09±0.49.2.83±0.96.7.57±1.01 kU/Lvs2.12±0.42 kU/L)和AI(4d组:50.5%±9.7%,48.9%±8.5%.63.5%±6.7%vs22.6%±3.3%:7d组:41.6%±7.8%.33.8%±5.1%.64.7%±10.4%vs 23.1%±5.4%)显著高于假手术对照组(P＜0.01),而EN-S和PRE-EN组的内毒素、DAO和AI显著低于相同时间点的PN组(P＜0.01);PRE-EN组的内毒素、DAO水平显著低于相同时间点的EN-S组(P＜0.01),而AI显著低于EN.S 7d组(P＜0.05):EN-S和PRE-EN 7d组与4d组相比,DAO水平和AI显著降低,内毒素水平有降低趋势,但未检出显著性差异.结论:添加益生元的微生态EN有助于维护SAP大鼠肠屏障功能,减少肠上皮细胞凋亡,减少内毒素易位的发生;EN在维护SAP大鼠肠屏障功能方面的作用优于PN.     

益生元对急性胰腺炎大鼠肠屏障功能的影响

目的 研究肠道补充益生元对急性胰腺炎肠上皮细胞紧密连接和屏障功能的影响.方法 Wistar大鼠腹腔注射左精氨酸建立AP模型,按随机数字法分组法分成对照组、AP组、益生元组.益生元组于造模前7 d开始给予益生元4 g·kg-1·d-1.建模后12 h处死大鼠,心脏取血检测血浆二胺氧化酶(DAO)活性,观察空肠病理变化、采用免疫组化方法检测紧密结合蛋白Occludin的含量.结果 AP组的血浆DAO活性为(7.29±0.68)U/L,显著高于对照组的(2.01±0.34)U/L(P＜0.01)和益生元组的(3.44±0.59)U/L(P＜0.05).AP组肠上皮occludin蛋白表达的灰度值为95.1±9.2,明显高于对照组的44.7±8.2和益生元组的59.7±7.8(P＜0.01).益生元组occludin表达也显著高于对照组(P＜0.05).结论 AP大鼠补充益生菌可增加肠上皮occludin蛋白表达,维持肠上皮紧密连接,维持正常的肠道通透性,从而达到保护肠黏膜屏障的效果.     

高迁移率族蛋白B1在重症急性胰腺炎肠屏障损害中的作用

目的:探讨高迁移率族蛋白B1在重症急性胰腺炎(SAP)肠屏障损害中的作用及其机制.方法:采用逆行胆胰管注射50 g/L牛磺胆酸钠制备SAP大鼠模型.将56只Wistar大鼠随机分为正常对照组(Control组),SAP 3h,6h,12h,24h,48h 5个亚组,二硫代氨基甲酸吡咯烷处理组(PDTC组),每组8只.PDTC组于建模后24h取材.测定血浆内毒素(LPs)、二胺氧化酶(DAO)水平,用逆转录-聚合酶链反应(RT-PCR)方法检测肠组织高迁移率族蛋白B1(HMGB1)mRNA表达,用Western blot法检测肠组织HMGB1水平.结果:与对照组比较,SAP 6h组大鼠肠组织HMGB 1 mRNA表达显著增高(0.41±0.06 vs 0.26±0.03,P<0.01),12h呈现进一步升高趋势,24h达峰值(0.62±0.06),并持续至48h.PDTC干预可显著降低肠组织HMGB1 mRNA表达(0.35±0.06 vs 0.62±0.06,P<0.01).PDTC组较SAP 24h组肠组织HMGB1 mRNA表达,血浆LPS和DAO显著下降(HMGB1 mRNA表达:0.35±0.06 vs 0.62±0.06,P<0.01;LPS:0.433±0.120 KEU/L vs 0.852±0.232 KEU/L,P<0.01;DAO:0.65±0.12 kU/L vs 1.36±0.22 kU/L,P<0.01).结论:SAP时,肠组织内HMGB1表达上调;PDTC可以明显抑制SAP时肠组织内HMGB1表达.     

急性重症胰腺炎肠黏膜屏障损伤机制与临床治疗进展

急性重症胰腺炎（SAP）是一种常见的临床急腹症,发病急,死亡率高。它可通过机体缺血缺氧、缺血一再灌注（IR）损伤、微生物屏障破坏、炎症介质的过度释放和表达、细胞凋亡等因素导致肠黏膜屏障功能的破坏并引发细菌移位和内毒素血症,甚至诱发全身炎症反应综合征（SIRS）和多器官脏器功能衰竭（MODS）。因此肠黏膜屏障的损伤与修复在急性重症胰腺炎病程进展及临床预防和治疗中有着特殊地位。本文将对急性重症胰腺炎疾病发展过程中肠黏膜屏障损伤的机制以及临床治疗进展作一概述。     

氧化苦参碱诱导跨膜蛋白Claudin-1表达在重症急性胰腺炎大鼠肠黏膜损害中的作用

目的:探讨氧化苦参碱(OM)在重症急性胰腺炎(SAP)肠黏膜屏障损害中的作用及其机制.方法:采用L-精氨酸(1 750 mg/kg)腹腔注射制备SAP大鼠模型.将80只Wistar大鼠随机分为Control组、OM对照组、SAP对照组、OM治疗组1、12、24、36、48 h 5个亚组,每组10只.分时取材,测定血浆内...     

Preventive effect of tetramethylpyrazine on intestinal mucosal injury in rats with acute necrotizing pancreatitis

INTRODUCTION Acute pancreatitis (AP) is often complicated by intestinal injury. However, its pathogenesis remains unclear. As we know, AP involves a complex array of mediators initiating and amplifying the systemic inflammatory response and therefore lead…     

Alterations of intestinal immune function and regulatory effects of L-arginine in experimental severe acute pancreatitis rats

ABM: To discuss the changes of intestinal mucosal immune function in rats with experimental severe acute pancreatitis (SAP) and the regulatory effect of L-arginine. METHODS: Male adult Wistar rats were randomly divided into pancreatitis group, sham-operation group, and L-arginine treatment group. Animals were killed at 24, 48, and 72 h after SAP models were developed and specimens were harvested. Endotoxin concentration in portal vein was determined by limulus endotoxin analysis kit. CD3+, CD4+, CD8+ T lymphocytes in intestinal mucosal lamina propria were examined by immunohistochemistry. Secretory immunoglobulin A (SIgA) in cecum feces was examined by radioimmunoassay. RESULTS: Compared to the control group, plasma endotoxin concentration in the portal vein increased, percentage of CD3+ and CD4+ T lymphocyte subsets in the end of intestinal mucosal lamina propria reduced significantly, CD4+/CD8+ ratio decreased, and SIgA concentrations in cecum feces reduced at 24, 48, and 72 h after SAP developed. Compared to SAP group, the L-arginine treatment group had a lower level of plasma endotoxin concentration in the portal vein, a higher CD3+ and CD4+ T lymphocyte percentage in the end of intestinal mucosal lamina propria, an increased ratio of CD4+/CD8+ and a higher SIgA concentration in cecum feces. CONCLUSION: Intestinal immune suppression occurs in the early stage of SAP rats, which may be the main reason for bacterial and endotoxin translocation. L-arginine can improve the intestinal immunity and reduce bacterial and endotoxin translocation in SAP rats.     

益生菌及肠内外营养对重症急性胰腺炎大鼠肠道黏附分子及免疫屏障的影响

目的:观察益生菌及肠外、肠内营养对重症急性胰腺炎(SAP)大鼠肠道黏附分子MAdCAM-1及免疫屏障的影响.方法:经胆胰管逆行注射50g/L牛磺胆酸钠制作SAP模型24h后,分别给予肠外营养(PN组),肠外 肠内营养(PN EN组),肠外 肠内营养 益生菌(益生菌组),持续6d,7d时处死,检测腹腔脏器组织菌群易位率,免疫组化法测定末端回肠和Peyer结MAdCAM-1,CD4,CD8,IgA.结果:益生菌组、PN EN组CD4、CD8T细胞数量及IgA,MAdCAM-1表达高于PN组(P<0.05);益生菌组Peyer结MAdCAM-1,CD8表达高于PN EN组(P<0.05).PN组菌群易位率(70.2%)、7d死亡率(75.6%)高于益生菌组(27.5%,50.0%)、PN EN组(30.5%,52.4%)(P<0.01或P<0.05),但后两组间差异无显著性意义.结论:EN能增加MAdCAM-1表达,提高SAP时肠免疫屏障,减少菌群易位,提高生存率.加用益生菌后总体改善不明显.     

Overexpressed miRNA-155 dysregulates intestinal epithelial apical junctional complex in severe acute pancreatitis

AIM:To investigate whether miRNA-155(miR-155)dysregulates apical junctional complex(AJC)protein expression in experimental severe acute pancreatitis(SAP).METHODS:Twenty-four male BALB/c mice were randomly assigned to two groups:the SAP group(n=12)receiving sequential intraperitoneal injection of 50μg/kg caerulein and 10 mg/kg lipopolysaccharide over 6h,and the control group(n=12)receiving intraperitoneal injection of normal saline.Animals were sacrificed3 h following the last injection for collection of blood samples and pancreas and distal ileal segment specimens.Routine pancreas and intestine histology was used to assess SAP pathology and intestinal epithelial barrier damage.Levels of serum amylase,diamine oxidase(DAO),and tumor necrosis factor(TNF)-αwere determined using commercial kits.Total RNA samples were isolated from intestinal epithelial specimens and reversely transcribed into cDNA.miR-155 and RhoA mRNA expression profiles were determined using quantitative real-time polymerase chain reaction.Target genes for miR-155 were predicted using the miRTarBase database,RNA22 and PicTar computational methods.Western blotting was performed to quantitate the protein expression levels of the target gene RhoA,as well as zonula occludens(ZO)-1 and E-cadherin,two AJC component proteins.RESULTS:Intraperitoneal injection of caerulein and lipopolysaccharide successfully induced experimental acute pancreatic damage(SAP vs control,10.0±2.0vs 3.2±1.2,P<0.01)and intestinal epithelial barrier damage(3.2±0.7 vs 1.4±0.7,P<0.01).Levels of serum amylase(21.6±5.1 U/mL vs 14.3±4.2 U/mL,P<0.01),DAO(21.4±4.1 mg/mL vs 2.6±0.8 mg/mL,P<0.01),and TNF-α(61.0±15.1 ng/mL vs 42.9±13.9 ng/mL,P<0.01)increased significantly in SAP mice compared to those in control mice.miR-155 was significantly overexpressed in SAP intestinal epithelia(1.94±0.50 fold vs 1.03±0.23 fold,P<0.01),and RhoA gene containing three miR-155-specific binding sites in the three prime untranslated regions was one of the target genes for mi     

肠道菌群失衡在急性胰腺炎肠黏膜屏障损伤中的作用

急性胰腺炎(acute pancreatitis,AP)是临床常见的急腹症,其发病率呈逐年增高趋势.AP病情进展迅速,15％～20％的患者发展为重症急性胰腺炎(severe acute pancreatitis,SAP),病死率高达20％～30％.SAP常可导致肠道功能障碍,包括肠黏膜屏障损伤和肠道动力障碍,引起肠道细...     

早期空肠内营养联合中药肠内滴注对重症急性胰腺炎患者肠麻痹的改善作用

目的:评价早期空肠内营养联合中药加味大承气颗粒肠内滴注治疗对改善重症急性胰腺炎患者肠麻痹的作用,探索重症急性胰腺炎的中西医结合治疗的新途径.方法:39例重症急性胰腺炎患者在常规治疗基础上,随机分成3组分别进行全胃肠外营养(PN组)、早期肠内营养(EN组)、肠内营养+中药大承气颗粒(EN+中药组)肠内滴注,观察患者腹痛腹胀缓解时间、胃肠道功能恢复(肠鸣音出现、肛门排气及排便)时间,并动态监测血淀粉酶、高敏C反应蛋白(CRP)、血浆肿瘤坏死因子-α(TNF-α).结果:EN组、EN+中药组患者经治疗后腹痛腹胀症状均缓解或消失,胃肠道功能恢复正常.PN组12例中,有2例腹胀、肠麻痹持续加重,其中1例出现腹腔隔室综合征并发多脏器功能衰竭.EN组、EN+中药组在腹胀(d)、腹痛缓解时间(d)以及胃肠道功能恢复时间(d)均优于PN组(4.22±0.94,3.02±0.75vs5.72±1.55;4.66±1.14,3.14±0.62vs6.81±1.81;3.42±0.82,3.21±0.88vs6.04±1.67,均P<0.05),其中EN+中药组腹胀(d)、腹痛缓解时间(d)优于EN组(3.02±0.75vs4.22...