急性坏死型胰腺炎 在 外科学 分类中 的翻译结果
本文关键词：大鼠急性坏死型胰腺炎病理特征评定方法的研究，由笔耕文化传播整理发布。
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Pathological Characteristics of Acute Necrotizing Pancreatitis in Rats and the Methods of Evaluation
大鼠急性坏死型胰腺炎病理特征评定方法的研究
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Role of apoptosis in the cell death of rat intestinal epithelium during the early stage of acute necrotizing pancreatitis
细胞凋亡在急性坏死型胰腺炎早期肠黏膜上皮细胞死亡中的作用
短句来源
Effects of glutamine on the intestinal failure in rats model of acute necrotizing pancreatitis
谷氨酰胺对急性坏死型胰腺炎大鼠肠道衰竭的治疗作用
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Protective effects of ulinostatin on acute lung injury induced by acute necrotizing pancreatitis in rats
乌司他丁对急性坏死型胰腺炎大鼠肺损伤的保护作用
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Effect of 5-fluorouracil on Exocrine of Pancreas in Dogs with Acute Necrotizing Pancreatitis
5-氟尿嘧啶对狗急性坏死型胰腺炎外分泌影响的研究
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Comparative analysis of ultrasonography and computerized tomography in the diagnosis of acute necrosis pancreatitis
急性坏死型胰腺炎超声与CT诊断对照分析
短句来源
Objective:To evaluate the diagnostic accuracy of ultrasonograp hy (US)and computerized tomography(CT)on acute necrosis pancreatitis(ANP).
目的评价超声与CT对急性坏死型胰腺炎(ANP)的诊断价值。
短句来源
Pathological Characteristics of Acute Necrotizing Pancreatitis in Rats and the Methods of Evaluation
大鼠急性坏死型胰腺炎病理特征评定方法的研究
短句来源
Role of apoptosis in the cell death of rat intestinal epithelium during the early stage of acute necrotizing pancreatitis
细胞凋亡在急性坏死型胰腺炎早期肠黏膜上皮细胞死亡中的作用
短句来源
Effects of glutamine on the intestinal failure in rats model of acute necrotizing pancreatitis
谷氨酰胺对急性坏死型胰腺炎大鼠肠道衰竭的治疗作用
短句来源
Protective effects of ulinostatin on acute lung injury induced by acute necrotizing pancreatitis in rats
乌司他丁对急性坏死型胰腺炎大鼠肺损伤的保护作用
短句来源
Effect of 5-fluorouracil on Exocrine of Pancreas in Dogs with Acute Necrotizing Pancreatitis
5-氟尿嘧啶对狗急性坏死型胰腺炎外分泌影响的研究
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Experience of the Drainage Tubes' Placement in the Operation of Acute Necrotising Pancreatitis (ANP)
急性坏死型胰腺炎术中置引流管的探讨
短句来源
Objective:To raise the clinical cure rate of acute necrotising pancreatitis (ANP), and to decrease the interrelated complications of the drainage tube.
目的 :提高急性坏死型胰腺炎 (ANP)临床治愈率 ,减少引流相关的并发症。
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acute necrotizing pancreatitis
The Penetration of Ciprofloxacin into Human Pancreatic and Peripancreatic Necroses in Acute Necrotizing Pancreatitis
The results showed that acute necrotizing pancreatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct.
The acute necrotizing pancreatitis model was not induced by injection of E.
Large pharmacological doses of ceruletide administered to conscious dogs by intravenous (i.v.) infusion uniformly induce a severe acute necrotizing pancreatitis within 4 h.
Serum concentrations of free fatty acids (FFA) were assayed in 20 patients with acute necrotizing pancreatitis (ANP).
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acute necrotizing pancreatitis
The Penetration of Ciprofloxacin into Human Pancreatic and Peripancreatic Necroses in Acute Necrotizing Pancreatitis
The results showed that acute necrotizing pancreatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct.
The acute necrotizing pancreatitis model was not induced by injection of E.
Large pharmacological doses of ceruletide administered to conscious dogs by intravenous (i.v.) infusion uniformly induce a severe acute necrotizing pancreatitis within 4 h.
Serum concentrations of free fatty acids (FFA) were assayed in 20 patients with acute necrotizing pancreatitis (ANP).
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acute necrotising pancreatitis
Acute necrotising pancreatitis-a role for enterokinase
The management of severe acute necrotising pancreatitis: an evidence-based review of the literature
The investigation of the effects of the celecoxib as a cylooxygenase-2 (COX-2) inhibitor on the course of the acute necrotising pancreatitis (ANP) in rats.
A 17-year-old boy with respiratory failure due to acute necrotising pancreatitis was admitted to our intensive care unit.
He presented with respiratory failure due to acute necrotising pancreatitis that developed five days after he had become ill.
Objective:To investigate the potential role of intestinal microflora barrier in the pathogenesis of pancreatic infection.Methods:Fifteen dogs were colonized with a strain of E.coli JM109 bearing ampicillinresistance plasmid PUC 18.The dogs were divided into two groups.In experimental group (n=8),acute necrotizing pancreatitis(ANP) was induced by injection of 0 5 ml/kg of sodium taurocholate with 3 000 U/kg trypsin into the pancreatic duct.The control group (n=7) underwent laparotomy only.All animals were sacrificed...
Objective:To investigate the potential role of intestinal microflora barrier in the pathogenesis of pancreatic infection.Methods:Fifteen dogs were colonized with a strain of E.coli JM109 bearing ampicillinresistance plasmid PUC 18.The dogs were divided into two groups.In experimental group (n=8),acute necrotizing pancreatitis(ANP) was induced by injection of 0 5 ml/kg of sodium taurocholate with 3 000 U/kg trypsin into the pancreatic duct.The control group (n=7) underwent laparotomy only.All animals were sacrificed 7 days later.Mucosal and luminal microflora of intestine were analyzed quantitatively,and various organs were harvested for culturing.Results:In the experimental group,population levels of E.coli in the intestine were much higher than those of the controls,while bifidobacterium and lactobacillus were decreased significantly (all P <0 01),resulting in reversal of bifidobacterium/E.coli ratio as compared with the control group ( P <0 05).In addition,intestinal bacteria was isolated from organs of all animals in the experimental group,and JM109 was also detected in most cases.Positive blood culture was 75 0% and 62 5% on day 1 and day 2 after induction of ANP respectively,but no bacteria was found in the controls.Conclusions:This study confirms that microecological disturbance can take place in ANP ,and overgrowth of intestinal gramnegative bacteria may lead to translocation to the pancreas and other organs,becoming the source of pancreatic and peripancreatic infection.
目的：探索肠道生物屏障改变在胰腺感染中的作用。方法：１５只杂种犬在定植耐氨苄青霉素大肠杆菌（携带质粒ＰＵＣ１８的ＪＭ１０９）后，随机分组。胰腺炎组（８只）胰管内注入５％牛磺胆酸钠和胰蛋白酶引发急性坏死型胰腺炎，对照组（７只）仅作单纯剖腹术，７天后活杀。定量分析肠道粘膜及内容物中的菌群数，且对血液和内脏进行细菌培养。结果：胰腺炎组肠粘膜及内容物中大肠杆菌计数均高于对照组（Ｐ＜０．０５或Ｐ＜０．０１），而双歧杆菌及乳杆菌均明显减少（Ｐ均＜０．０１）；肠粘膜厌氧菌／需氧菌比值严重倒置（Ｐ＜０．０５）；脏器和血培养结果：胰腺炎组所有动物均出现了肠道细菌易位，以肠系膜淋巴结和胰腺易位率最高（８７．５％～１００．０％），且能找到术前人工定植于肠道的耐药质粒菌。胰腺炎后第１天和第２天血培养阳性率分别为７５．０％和６２．５％，而对照组全部阴性。结论：急性坏死型胰腺炎时肠道出现明显的细菌微生态失调，以过度生长的Ｇ－杆菌为主的肠道细菌易位到胰腺及其它脏器，成为胰腺及胰周感染的根源。
Objective To investigate whether apoptosis of intestinal epithelial cells occurs at the early stage of acute necrotizing pancreatitis (ANP) in rats. Methods Fourty eight Spraque Dawley rats were used. ANP model of rats was induced by retro injection of 5% sodium taurocholate into biliopancreatic duct. Laparotomized animals without induction of ANP (sham operation) served as controls. The distal segment of ileum specimens were harvested at 3 h, 6 h, 12 h and 24 h after operation and the apoptosis of intestinal...
Objective To investigate whether apoptosis of intestinal epithelial cells occurs at the early stage of acute necrotizing pancreatitis (ANP) in rats. Methods Fourty eight Spraque Dawley rats were used. ANP model of rats was induced by retro injection of 5% sodium taurocholate into biliopancreatic duct. Laparotomized animals without induction of ANP (sham operation) served as controls. The distal segment of ileum specimens were harvested at 3 h, 6 h, 12 h and 24 h after operation and the apoptosis of intestinal epithelial cells was studied by DNA gel electrophoresis, FITC conjugated annexin V and propidium iodide (PI) staining cells analyzed by Flow Cytometry (FCM) and immunohistochemical procedures (TUNEL method). Results The DNA electrophoresis showed that typical “ladder” patterns appeared at all indicated time points in ANP group, while the DNA specimens from control group presented a single chromosomal lane, except the one at 12 h. Apoptotic percentage of detached intestinal epithelial cells assayed using Annexin V kit by FCM were (53.7±3.7)%, (27.6±6.0)%, (39.0±4.8)%, (29.0±11.3)% at 3 h, 6 h, 12 h and 24 h in control group and (50.3±11.3)%, (79.7±9.2)%, (47.8±17.3)%, (49.6±9.5)% in ANP group. There was a significant difference between two groups at 6 h, P <0.05. The ratio of apoptotic cells and necrotic cells (A/N) was 27.7±17.9. Apoptotic index determined by TUNEL method were significantly increased in ANP group (17.5±3.5, 20.4 ±2.9, 14.8±1.7, 14.2±2.1) compared with control group (6.2±2.4, 7.5±1.7, 10.5±0.9, 5.3 ± 0.8 ) during all observed period, P <0.01, peaked at 6 h. Conclusions It was suggested that apoptosis of intestinal epithelial cells increased at early stage of ANP in rat, especially at 6 h. Apoptosis is a principle model of cell death in rat intestinal epithelium of ANP. These might be involved in the development of intestinal barrier failure during the course of ANP.
目的 观察急性坏死型胰腺炎 (ANP)大鼠早期肠黏膜上皮细胞凋亡的发生及其演变规律 ,探讨其在肠黏膜屏障功能障碍中的作用。方法 Spraque Dawley大鼠 48只 ,采用胆胰管内逆行注入5 %牛磺胆酸钠溶液诱导大鼠ANP模型。假手术组 (shamoperation ,SO)大鼠仅作剖腹术。术后 3、6、12和 2 4h分批处死大鼠 ,取末端回肠组织 ,分别应用DNA琼脂糖凝胶电泳 ,异硫氰基荧光素 (FITC)结合的Annexin V和碘化丙啶 (PI)标记细胞作流式细胞仪 (FCM)检测和免疫组化 (TUNEL法 )等技术 ,研究ANP大鼠肠黏膜上皮细胞凋亡。结果 DNA琼脂糖凝胶电泳结果显示 ,SO组仅于 12h出现“梯形(ladder)”条带 ;ANP大鼠 ,各时点均可见“梯形”条带。FCM检测结果表明 ,术后 3、6、12和 2 4hSO组肠黏膜上皮脱落细胞凋亡比例分别为 (5 3 .7± 3 .7) %、(2 7.6± 6 .0 ) %、(39.0± 4.8) %和 (2 9.0± 11.3) % ;ANP组分别为 (5 0 .3± 11.3) %、(79.7± 9.2 ) %、(...
目的 观察急性坏死型胰腺炎 (ANP)大鼠早期肠黏膜上皮细胞凋亡的发生及其演变规律 ,探讨其在肠黏膜屏障功能障碍中的作用。方法 Spraque Dawley大鼠 48只 ,采用胆胰管内逆行注入5 %牛磺胆酸钠溶液诱导大鼠ANP模型。假手术组 (shamoperation ,SO)大鼠仅作剖腹术。术后 3、6、12和 2 4h分批处死大鼠 ,取末端回肠组织 ,分别应用DNA琼脂糖凝胶电泳 ,异硫氰基荧光素 (FITC)结合的Annexin V和碘化丙啶 (PI)标记细胞作流式细胞仪 (FCM)检测和免疫组化 (TUNEL法 )等技术 ,研究ANP大鼠肠黏膜上皮细胞凋亡。结果 DNA琼脂糖凝胶电泳结果显示 ,SO组仅于 12h出现“梯形(ladder)”条带 ;ANP大鼠 ,各时点均可见“梯形”条带。FCM检测结果表明 ,术后 3、6、12和 2 4hSO组肠黏膜上皮脱落细胞凋亡比例分别为 (5 3 .7± 3 .7) %、(2 7.6± 6 .0 ) %、(39.0± 4.8) %和 (2 9.0± 11.3) % ;ANP组分别为 (5 0 .3± 11.3) %、(79.7± 9.2 ) %、(4 7.8± 17.3) %和 (4 9.6± 9.5 ) % ,术后 6h达峰值 ,且较SO组明显增高 (P <0 .0 1) ,凋亡与坏死细胞 (A/N)比值为 2 7.7± 17.9。TUNEL法显示 ,凋亡细胞呈细胞核固缩、断片状 ,术后 3、6、12和 2 4hSO组凋亡指数为 6 .2± 2 .4、7.5± 1.7、10 .5± 0 .9和 5 .3± 0 .8;ANP组为 1
Objective To determine the effects of glutamine (Gln) on the intestinal failure in rats with acute necrotizing pancreatitis (ANP) and its possible mechanisms. Methods Fifty-four Spraque-Dawley rats were randomly divided into 3 groups: sham operation (SO, n=18), ANP (n=18), and ANP treated with Gln (ANP+Gln, n=18). ANP model was induced by injection of 5% sodium taurocholate solution into bilo-pancreatic duct. The therapy was continuously given with amino acid solution by a mini-pump via a central intravenous...
Objective To determine the effects of glutamine (Gln) on the intestinal failure in rats with acute necrotizing pancreatitis (ANP) and its possible mechanisms. Methods Fifty-four Spraque-Dawley rats were randomly divided into 3 groups: sham operation (SO, n=18), ANP (n=18), and ANP treated with Gln (ANP+Gln, n=18). ANP model was induced by injection of 5% sodium taurocholate solution into bilo-pancreatic duct. The therapy was continuously given with amino acid solution by a mini-pump via a central intravenous line. In addition, the ANP+Gln group was received 3% Gln dipeptide solution (equal to 2% Gln) with a dosage of 0.5g·kg -1·d -1. These groups were isocaloric and isonitrogenous. Bacterial cultures from pancreas, mesenteric lymph node (MLN), liver, spleen and acites were done at 24, 48, 72 h after operation. Endotoxin level in portal vein was determined. Pathologic changes of intestinal mucosa were also studied. Apoptosis of intestinal mucosa was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method. Expressions of insulin-like growth factor 1 (IGF-1), Gln synthetase (GSase) and glutaminase (Glnase) mRNA were assayed by reverse transcription polymerase chain reaction (RT-PCR). Results At 24, 48, 72h, the positive rate of bacterial culture and the endotoxin concentration were increased significantly in ANP group compared to the SO group (P<0.05), while Gln could decrease them significantly. Pathologic study showed that the height of mucosal villous in ANP group was lower than that in SO group, indicating the intestinal mucosa became more atrophy. However ,the height of mucosal villous in ANP+Gln group was no significantly difference compared to that in SO group, indicated Gln could preserve the mucosa well. Apoptotic index was increased in ANP group and decreased in Gln treated rats. Expressions of IGF-1, GSase, Glnase mRNA were down-regulated in ANP group, but were up-regulated in ANP+Gln group. Conclusions The intestinal barrier function was impaired in ANP. Gln could protect intestinal barrier function. This action was probably related to its enhancement of IGF-1, GSase and Glnase mRNA expressions and its inhibition of intestinal mucosal apoptosis.
目的 观察谷氨酰胺 (Gln)对急性坏死型胰腺炎 (ANP)大鼠肠道衰竭的治疗作用 ,并探讨其作用机制。方法 Spraque Dawley大鼠 5 4只 ,随机分为假手术组 (SO)、ANP组、Gln治疗组 (ANP +Gln) ,每组 18只。采用 5 %牛磺胆酸钠溶液经胆胰管内逆行注射诱导大鼠ANP模型。大鼠中心静脉置管 ,用微量输液泵输注含等氮、等热卡的氨基酸溶液 ,ANP +Gln组加入 3%丙氨酸 Gln双肽 (相当于2 %Gln溶液 ,剂量 0 5g·kg-1·d-1)。术后 2 4、48、72h分批处死大鼠并留取标本 ,分别做肠黏膜组织病理检查 ,肝、胰、脾、肠系膜淋巴结 (MLN)和腹水等组织细菌培养 ,门静脉血内毒素测定 ,TUNEL法检测肠黏膜上皮细胞凋亡 ;逆转录 聚合酶链反应研究肠黏膜组织胰岛素样生长因子 1(IGF 1)、Gln酶和Gln合成酶mRNA表达。结果 SO组大鼠各组织培养均无阳性细菌 ,ANP组细菌培养阳性率明显高于SO组 ,P <0 0 5 ,以MLN阳性率最高 ;ANP +Gln组细菌培养阳性率则显著低于ANP组 ,P <0 0 5。血浆内毒素在A...
目的 观察谷氨酰胺 (Gln)对急性坏死型胰腺炎 (ANP)大鼠肠道衰竭的治疗作用 ,并探讨其作用机制。方法 Spraque Dawley大鼠 5 4只 ,随机分为假手术组 (SO)、ANP组、Gln治疗组 (ANP +Gln) ,每组 18只。采用 5 %牛磺胆酸钠溶液经胆胰管内逆行注射诱导大鼠ANP模型。大鼠中心静脉置管 ,用微量输液泵输注含等氮、等热卡的氨基酸溶液 ,ANP +Gln组加入 3%丙氨酸 Gln双肽 (相当于2 %Gln溶液 ,剂量 0 5g·kg-1·d-1)。术后 2 4、48、72h分批处死大鼠并留取标本 ,分别做肠黏膜组织病理检查 ,肝、胰、脾、肠系膜淋巴结 (MLN)和腹水等组织细菌培养 ,门静脉血内毒素测定 ,TUNEL法检测肠黏膜上皮细胞凋亡 ;逆转录 聚合酶链反应研究肠黏膜组织胰岛素样生长因子 1(IGF 1)、Gln酶和Gln合成酶mRNA表达。结果 SO组大鼠各组织培养均无阳性细菌 ,ANP组细菌培养阳性率明显高于SO组 ,P <0 0 5 ,以MLN阳性率最高 ;ANP +Gln组细菌培养阳性率则显著低于ANP组 ,P <0 0 5。血浆内毒素在ANP组明显高于SO组 (P <0 0 5 ) ,且随着时间延长而递升 ;ANP +Gln组血浆内毒素较ANP组显著下降 (P <0 0 5 )。ANP组肠黏膜绒毛高度显著低于SO组 (P <0 0 5 ) ,提示ANP时肠黏膜处于萎缩状态 ,而ANP +Gln组较SO组则差异无显著性 (P >0 0 5 )
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本文关键词：大鼠急性坏死型胰腺炎病理特征评定方法的研究，由笔耕文化传播整理发布。
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