生长抑制和头孢噻甲羧肟对急性出血坏死性胰腺炎早期细菌移 …

为探讨急性出血坏死性胰腺炎感染的防治，我们观察了头孢噻羧肟和生长抑制素对ＡＨＮＰ早期细菌移位的影响。结果提示生长抑制素具有肠粘膜屏障保护作用，可能与其清除肠道氧自由基有关。我们还发现ＡＨＮＰ早期应用抗生素可减轻血行的细菌移位。     

急性出血坏死性胰腺炎早期细菌、内毒素易位及甘遂治疗作用的实验研究

以犬的急性出血坏死性胰腺炎（ＡＨＮＰ）模型为研究对象，观察ＡＨＮＰ早期细菌、内在素易位的动态及中药甘遂对ＡＨＮＰ早期细菌、内毒素易位的治疗作用。实验分为３组：ＡＨＮＰ对照组；ＡＨＮＰ甘遂处理组；健康对照组。结果显示ＡＨＮＰ早期即存在细菌、内毒素易位；中药甘遂不仅能阻碍ＡＨＮＰ早期细菌、内毒素易位，而且可以通过降低血中肿瘤坏死因子（ＴＮＦ）、磷脂酶Ａ２（ＰＬＡ２）等改变ＡＨＮＰ的病理生理过程，对ＡＨＮＰ有一定治疗作用。健康对照组各观察指标均无阳性发现，说明麻醉、手术操作对细菌、内毒素易位影响不大。     

急性出血坏死性胰腺炎早期细菌,内毒素易位及甘遂治疗作用的实…

以犬的急性出血坏死性胰腺炎模型为研究对象，观察ＡＮＨＰ早期细菌，内毒素易位的动态及中药城遂对ＡＨＮＰ早期细菌，内毒素易位的治疗作用。实验分为３组；ＡＨＮＰ对照组；ＡＨＮＰ甘遂处理组；健康对照组。结果显示ＡＨＮＰ－早期即存在细菌，内毒素易位；中药甘遂不仅能障碍ＡＨＮＰ早期细菌，内毒素易位，而且可以通过降低血中肿瘤坏死因子，磷脂酶Ａ２（ＰＬＡ２）等改变ＡＮＨＰ的病理生理过程，对ＡＨＮＰ有一定治疗作用。     

急性出血坏死性胰腺炎的诊断进展

急性出血坏死性胰腺炎（ＡＨＮＰ）是一种发病急、进展快、并发症多、治疗棘手的常见危重急腹症。文献报道,ＡＨＮＰ的病死率高达４０％～７０％（１,２）。因此,要降低其病死率,提高ＡＨＮＰ的早期诊断是关键之一。本文就ＡＨＮＰ的诊断进展综述如下。１临床诊断及诊...     

血小板活化因子拮抗剂对急性出血坏死性胰腺炎大鼠内毒素血症防治作用实验研究

采用去氧胆酸逆行胰管内注射法复制急性出血坏死胰腺炎（简称ＡＨＮＰ）大鼠模型，观察血小板活化因子（ＰＡＦ）拮抗剂对ＡＨＮＰ大鼠内毒素血症的防治作用。结果显示：ＡＨＮＰ后，血中ＰＡＦ和内毒素水平明显升高，两者呈正相关关系。应用ＰＡＦ拮抗剂后，ＰＡＦ和内毒素水平明显下降，同时也明显减轻了ＡＨＮＰ大鼠胰腺和肠粘膜的损害。实验结果提示，ＰＡＦ参与了ＡＨＮＰ大鼠内毒素血症的发病过程，应用ＰＡＦ拮抗剂对ＡＨＮＰ大鼠内毒素血症有良好的防治作用。     

急性重症胰腺炎26例治疗体会

近年来 ,我国急性胰腺炎的发病率仍呈上升趋势 ,治疗效果不能令人满意 ,尤其是急性重症胰腺炎 (ＡＨＮＰ)病情凶险 ,发展迅速 ,并发症多 ,死亡率高达 30 %～ 40 % [1 ] 。我院 1989～ 1999年共收治ＡＨＮＰ 2 6例 ,疗效较好 ,现报告如下。1　临床资料　　本组男 9例 ,女 17例 ,年龄 37～ 72岁。根据临床表现 ,生化指标 ,Ｂ超等检查 ,诊断均符合ＡＨＮＰ诊断标准[2 ] 。手术前全部行诊断性腹腔穿刺 ,2 1例抽得血性腹水 ,5例阴性 ;全部行血、尿淀粉酶测定 ,18例血和 (或 )尿淀粉酶升高。早期手术治疗 2 5例 ,均证实为ＡＨＮＰ ,腹腔渗液为混浊…     

急性出血坏死性胰腺炎早期血液内毒素,肿瘤坏死因子变化实验研究

有关急性出血坏死性胰腺炎（ＡＨＮＰ）早期血液内毒素、肿瘤坏死因子的变化规律目前报道不多，本研究旨在阐明这一问题，并探索中药甘遂对ＡＨＮＰ早期血液内毒素、ＴＮＦ的影响。１　材料和方法１．１　主要试剂、仪器：牛胆酸钠，为美国ｓｉｇｍａ公司产品；卵磷脂，为美国ｓｉｇｍａ公司产品；细菌内毒素微量定量试剂盒，为上海医学化验所提供，灵敏度为０．０３Ｅｕ／ｎｕ；肿瘤坏死因子酶联免疫检测试剂盒，由解放军军事医学科学院帮定公司提供，灵敏度为１００～６０ｐｇ／ｎｕ。ＢＩＯＴＥＫＩＮＳＴＲＯＭＥＮＴＳＥＬ３０９ｍｉ…     

低分子右旋糖酐对急性胰腺炎大鼠胰腺微血流的影响及其治…

目的：探讨低分子右旋糖酐对急性胰腺炎大鼠胰腺微区血流的影响及其对胰腺炎的治疗作用。方法：用５％牛磺胆酸钠诱发大鼠急性出血坏死性胰腺炎（ＡＨＮＰ）模型，并应用低分子右旋糖酐治疗，观察其对ＡＨＮＰ时平均动脉压、胰腺微区血流量、血清淀粉酶和脂肪酶及胰腺病理形态的影响。结果：ＡＨＮＰ早期在不影响平均动脉压的情况下，低分子右旋糖酐能显著增加胰腺微区血流量，并进一步降低血清淀粉酶和脂肪酶及减轻胰腺炎的病理改变     

生长抑素十四肽对大鼠胰腺炎微循环的影响

目的：在建立ＡＨＮＰ的大鼠模型基础上,初步研究急性胰腺炎（ＡＰ）的成因及药物对其的治疗作用。方法：利用微循环技术观察微血管口径、密度、血流速度、血流状态、微区血流量及治疗前后胰淀粉酶的变化及其光镜、电镜的超微病理学改变。结果：生长抑素十四肽组微循环各项指标的改善较模型组差异显著（Ｐ＜０．０１）,胰腺病变程度显著轻于病理对照组。结论：胰腺微循环的障碍可导致ＡＰ的发生,而生长抑素十四肽能有效地改善胰腺微循环而达到治疗目的。     

急性出血坏死性胰腺炎犬十二指肠液的返流

目的：观察急性出血坏死性胰腺炎（ＡＨＮＰ）发生以后,肠胰返流是否发生。方法：向犬的胰管中注入自身胆汁和１％胰蛋白酶,制成ＡＨＮＰ模型,关腹前行十二指肠造瘘并夹闭造瘘管。对４只ＡＨＮＰ犬和４只对照犬,向十二指肠闭袢内注入泛影葡胺和印度墨水的混合液,保持十二指肠压力为４ｋＰａ,观察是否有肠胰返流发生,并测量十二指肠压力变化。结果：４只ＡＨＮＰ犬中３只胰管显影,组织学切片观察４只ＡＨＮＰ犬的小胰管中均有墨水颗粒,但４只对照犬未见返流发生。ＡＨＮＰ发生以后,十二指肠内压迅速升高。结论：ＡＨＮＰ发生以后,由于肝胰壶腹括约肌功能障碍和十二指肠内高压,十二指肠液会持续地返流入胰管     

一氧化氮对内毒素血症大鼠肠道损伤及细菌移位的影响

目的 一氧化氮（NO）参与休克的血管扩张,血压下降,但它对组织损伤,特别是肠道的损伤及细菌移位的作用仍不十分清楚。本实验以NO合酶（NOS）底物左旋精氨酸及其抑制剂硝基左旋精氨酸（LNNA）为工具,观察NO对内毒素血症时大鼠肠道损伤及细菌移位的影响。方法 用内毒素（LPS,10mg/kg,ip）复制内毒素血症模型,给予LNNA或L-arg抑制或促进NO合成,测定肠道质过氧化物丙二醛（MDA)的含量,二胺氧化酶（DAD）活性及肠系膜淋巴结细菌培养。结果 LPS可降低肠细胞DAO活性,增加MDA含量和肠系膜淋巴细菌移位的发生率和细菌数量;用LNNA抑制NO后可加重LPS的上述作用,而给予L－arg促进NO合成则可减轻LPS的作用。结论 本实验结果表明在内毒素血症时,抑制NO可加重肠道损伤和细菌移位的发生,提示NO对肠组织有一定的保护作用。     

Role of granulocyte colony-stimulating factor in paclitaxel-induced intestinal barrier breakdown and bacterial translocation in rats

Background  Chemotherapy causes breakdown of the intestinal barrier, which may lead to bacterial translocation. Paclitaxel, an anti-tubulin agent, has many side effects; however, its effect on the intestinal barrier is unknown. Previous studies show that granulocyte colony-stimulating factor (G-CSF) plays an important role in modulating intestinal barrier function, but these studies are not conclusive. Here, we investigated the effects of paclitaxel on the intestinal barrier, and whether G-CSF could prevent paclitaxel-induced bacterial translocation.

Methods  Twenty-four male Sprague-Dawley rats were divided into three groups: control group, paclitaxel group and paclitaxel + G-CSF group. Intestinal permeability was measured by the urinary excretion rates of lactulose and mannitol administered by gavage. The mesenteric lymph nodes, spleen and liver were aseptically harvested for bacterial culture. Endotoxin levels and white blood cell (WBC) counts were measured and bacterial quantification performed using relative real-time PCR. Jejunum samples were also obtained for histological observation. Intestinal apoptosis was evaluated using a fragmented DNA assay and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP)-biotin nick end-labeling staining. One-way analysis of variance and Fisher’s exact test were used to compare differences between groups.

Results  Paclitaxel induced apoptosis in 12.5% of jejunum villus cells, which was reduced to 3.8% by G-CSF treatment. Apoptosis in the control group was 0.6%. Paclitaxel treatment also resulted in villus atrophy, increased intestinal permeability and a reduction in the WBC count. G-CSF treatment resulted in increased villus height and returned WBC counts to normal levels. No bacterial translocation was detected in the control group, whereas 6/8, 8/8, and 8/8 rats in the paclitaxel group were culture-positive in the liver, spleen and mesenteric lymph nodes, respectively. Bacterial translocation was partially inhibited by G-CSF.

Conclusions  Paclitaxel disrupts the intestinal barrier, resulting in bacterial translocation. G-CSF treatment protects the intestinal barrier, prevents bacterial translocation, and attenuates paclitaxel-induced intestinal side-effects.

     

表皮生长因子、谷氨酰胺强化的全胃肠外营养对肠屏障功能和肠细菌移位的影响

目的探讨表皮生长因子(epidermalgrowthfactor,EGF)、谷氨酰胺(glutamine,GLN)对全胃肠外营养(totalparenteralnutrition,TPN)并发症的防治作用及机制。方法将大白鼠分为4组A(正常喂养组)、B(标准胃肠外营养STPN)、C(TPN+GLN)、D(TPN+EGF+GLN),采用大白鼠TPN模型,一周后取大鼠近端空肠组织切片行光镜和电镜观察,结合图像分析;无菌采取肠系膜淋巴结(mesenterlymphonodus,MLN)并称重和抽取腹腔静脉血作细菌培养(需氧培养)。结果B组肠黏膜萎缩,MLN细菌培养阳性率62.5%。C组较B组肠黏膜萎缩减轻,黏膜DNA、RNA含量和浆细胞数目增加,MLN细菌培养阳性率37.5%,肠细菌移位率下降。而D组上述各指数与正常鼠A组无显著差异。4组动物血培养均为阴性。结论EGF和GLN联合应用能有效地保护肠屏障功能和防止肠细菌移位     

STUDY ON INHIBITION OF PANCREATIC EXOCRINE SECRETION BY SOMATOSTATIN IN RATS

We used a potent and specific monocional antibody to somatostatin to test the physiologoic inhibitory role of the tetradecapeptide somatostation on pancreatic secretion, Somatostatlncreased both the total amylase and vofume of pancreatic sectetion. C.hoIecystokirfin-A receptor antagom smabolished the stimulatory ellect of somatostatin Jmmunoneutralization, We conclude that somatotation tccli-tally inhiblts pancreatic secretion in fasted rats via inhibition of the release or action of cholecystokinin.,Furthermore, the source of these paptides is likely islet delta cells and intrapancxeatie neurons, respectively.     

中药大黄在机械通气治疗中的作用

中药大黄因为具有治疗呼吸衰竭,保护胃肠道,减少呼吸机相关肺炎及肺损伤等作用,已逐步应用于机械通气患者的辅助治疗。目前多项临床研究证实,大黄对机械通气患者的治疗有积极作用,并且可以调节免疫、抑制肠道细菌移位、抑制全身炎性反应综合征等。为此,对大黄的相关作用与其在机械通气中的应用情况予以综述。     

益生菌对炎症性肠病小鼠肠道菌群紊乱及细菌移位的影响

目的探讨植物乳杆菌（LP）对炎症性肠病（IBD）小鼠肠道菌群及细菌移位的影响。方法采用白介素10基因敲除（IL-10^-/-）小鼠作为IBD动物模型,将8周龄雌性小鼠随机分成空白对照组、IL-10^-/-组和IL—10^-/- ＋LP组三组。IL-10^-/- ＋LP组每日灌胃0．5mLLP菌液（1．0×10^9 CFU／mL）,其余两组灌胃Ringer缓冲液0．5mL,持续4周。以小鼠粪便中的双歧杆菌、乳酸杆菌、肠杆菌和产气荚膜梭菌数量及肠系膜淋巴结、脾脏细菌移位为检测指标。结果IL-10^-/-小鼠肠内双歧杆菌、乳酸杆菌含量明显下降,肠球菌、产气荚膜梭菌含量升高,且肠道细菌移位明显增加;而连续灌胃LP菌液4周后,益生菌发挥了对肠道的调节作用,纠正了肠道菌群失衡,并降低了肠道细菌移位。结论LP能纠正炎症性肠病小鼠肠道菌群紊乱,减少细菌移位,从而增强了肠道屏障功能。     

依达拉奉在大鼠失血性休克中保护机制的研究

目的:探究依达拉奉(Edaravone)在大鼠失血性休克引起的肠内菌群易位中作用机制。方法:大鼠在诱导休克后30及60min处死,肠系膜淋巴结取材检测菌群易位。血浆丝浆蛋白SLP试验检测细菌粘肽、β-葡聚糖及内毒素。4-HNE(4-hydroxy-2-nonenal)免疫组化染色评估休克后脂质过氧化反应程度。结果:依达拉奉可以降低失血性休克诱导的肠系膜淋巴结菌群易位。失血性休克导致的血浆丝浆蛋白水平增高同样可以被依达拉奉抑制。结论:在大鼠失血性休克时,依达拉奉可能降低肠内中性粒细胞参与的脂质过氧化反应引起的菌群易位。     

Effect of ecoimmunonutrition supports on maintenance of integrity of intestinal mucosal barrier in severe acute pancreatitis in dogs

Background One of the major causes of death in severe acute pancreatitis （SAP） is severe infection owing to bacterial translocation. Some clinical studies suggested that ecoimmunonutrition （EIN） as a new strategy had better treatment effect on SAP patients. But the experiment studies on the precise mechanism of the effect of EIN were less reported. In this study, we mainly investigated the effects of EIN on bacterial translocation in SAP model of dogs. Methods SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in healthy hybrid dogs. The SAP dogs were supported with either parenteral nutrition （PN） or elemental enteral nutrition （EEN） or EIN. The levels of serum amylase, serum aminotransferase and plasma endotoxin were detected before and after pancreatitis induction. On the 7th day after nutrition supports, peritoneal fluid, mesenteric lymph nodes （MLN）, liver, and pancreas were collected for bacterial culture with standard techniques to observe the incidence of bacterial translocation. Pathology changes of pancreas were analyzed by histopathologic grading and scoring of the severity of pancreas, and the degree of intestinal mucosal damage was assessed by measuring mucosal thickness, villus height, and crypt depth of ileum. Results Compared with PN and EEN, EIN significantly decreased the levels of serum amylase, serum aminotransferase, plasma endotoxin, and the incidence of bacterial translocation. Furthermore, compared with the others, the histology scores of inflammation in pancreas and the ileum injury （ileum mocosa thickness, villus height, and crypt depth） were significantly alleviated by EIN （P〈0.05）. Moreover, concerning liver function, the serum levels of alanine aminotransferase, aspartate aminotransferase and albumin were ameliorating significantly in the EIN group. Conclusion Our results suggested that EIN could maintain the integrity of intestinal mucosal barrier and reducing the incidence of bacterial translocation in SAP dogs. Early EIN was safe and more effective treatment for SAP dogs.     

益生菌对炎症性肠病小鼠肠道菌群紊乱及细菌移位的影响

目的 探讨植物乳杆菌(LP)对炎症性肠病(IBD)小鼠肠道菌群及细菌移位的影响.方法 采用白介素10基因敲除(IL-10~(-/-))小鼠作为IBD动物模型,将8周龄雌性小鼠随机分成空白对照组、IL-10~(-/-)组和IL-10~(-/-)+LP组三组.IL-10~(-/-)+LP组每日灌胃0.5 mL LP菌液(1.0×10~9CFU/mL),其余两组灌胃Ringer缓冲液0.5 mL,持续4周.以小鼠粪便中的双歧杆菌、乳酸杆菌、肠杆菌和产气荚膜梭菌数量及肠系膜淋巴结、脾脏细菌移位为检测指标.结果 IL-10~(-/-)小鼠肠内双歧杆菌、乳酸杆菌含量明显下降,肠球菌、产气荚膜梭菌含量升高,且肠道细菌移位明显增加;而连续灌胃LP菌液4周后,益生菌发挥了对肠道的调节作用,纠正了肠道菌群失衡,并降低了肠道细菌移位.结论 LP能纠正炎症性肠病小鼠肠道菌群紊乱,减少细菌移位,从而增强了肠道屏障功能.     

表皮生长因子减少腹部辐射肠外营养大鼠肠道细菌移位

观察表皮生长因子对接受长期全肠外营养的腹部辐射大鼠肠道细菌移位的影响,探讨其机制。方法应用ＴＳＢ培养,图像分析,高效液相色谱等方法检测应用ＧＥＦ后大鼠死亡率,肠粘膜形态结构,肠道细菌移位,血浆及组织谷氨酰胺水平及肠道Ｇｌｎ摄取率。结果应用ＥＧＦ后,大鼠钫率显降低,肠粘膜结构屏障改善,细胞移位减少,血液及组织Ｇｌｎ水平提高。结论ＥＧＦ在长期菌ＴＰＮ显改善辐射性肠粘膜屏障损伤大鼠营养的同时,减少Ｔ