lactulose和glutamine对梗阻性黄疸大鼠空肠黏膜的影响

目的:研究梗阻性黄疸时空肠黏膜的变化及lactulose和glutamine对梗阻性黄疸大鼠空肠黏膜的影响．方法:Wistar大鼠84只,随机分为4组．通过手术结扎切断大鼠胆总管得到梗阻性黄疸模型．对梗阻性黄疸大鼠分别经胃灌注lactulose和glutamine药物,比较给药前及给药后5,10 d各组大鼠空肠黏膜绒毛高度变化,同时与未行胆管结扎的假手术对照组进行比较．结果:无论胆总管结扎与否,给药前各组空肠黏膜的绒毛高度无明显差异．胆总管结扎后大鼠空肠黏膜高度减低(5 d:q=4．32,P<0．01;10 d:q=11．03,P<0．01);应用生理盐水组大鼠的空肠黏膜绒毛高度明显低于应用lactulose和glutamine组大鼠的空肠黏膜绒毛高度,且应用glutamine组与胆总管未结扎组相近(5 d:q= 3．62,P>0．05;10 d:q=3．83,P>0．05);而应用lactulose和glutamine的2组大鼠空肠黏膜绒毛高度无明显差异(P>0．05)．结论:结扎大鼠胆总管可导致其空肠黏膜萎缩．经胃肠道应用lactulose或glutamine对胆道梗阻所致的大鼠空肠黏膜萎缩均具有保护作用,且二者对肠黏膜的保护作用无明显差异．     

梗阻性黄疸对大鼠周围神经结构的影响

将30只Wistar大鼠随机分为对照组、假手术组、梗阻性黄疸（OJ）组,每组10只。OJ组大鼠于近肝门处游离并结扎胆总管,假手术组仅做游离但不结扎胆总管。对照组、假手术组大鼠术后体质量上升,OJ组体质量显著降低,与术前相比P均〈0.05。OJ组大鼠术后血清直接胆红素、胆汁酸、内毒素水平显著高于正常对照组和假手术组,P均〈0.01。OJ组神经损伤较重。认为梗阻性黄疸大鼠存在周围神经变性,与内毒素移位和高胆红素血症有关。     

阻塞性黄疸大鼠肝组织Bcl-2及BaX的表达与细胞凋亡

目的探讨在阻塞性黄疸肝损害中Bcl-2,Bax基因的表达.方法结扎Wistar大鼠胆总管建立阻塞性黄疸大鼠动物模型.分为结扎后3,7,14,21d及阴性对照各组,每组8只.结扎后3,7,14,21 d处死大鼠,门静脉抽血,离心后取上层血清行胆红素测定.HE染色,光镜下观察阻塞性黄疸大鼠肝脏组织的病理改变.用末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记技术(TUNEL)和免疫组织化学方法检测阻塞性黄疸大鼠肝脏组织细胞凋亡状态及凋亡相关基因Bcl-2,Bax蛋白的表达.结果胆总管结扎后,随结扎时间的延长胆红素值逐渐增高.光镜下,胆总管结扎3d即见肝内胆管扩张,结扎7 d,肝细胞内或细胞间瘀胆,纤维组织增生;结扎14 d,纤维组织增生向肝小叶内扩展;结扎21 d,纤维组织带增宽,肝脏结构广泛改变.TUNEL检测表明,正常大鼠肝组织偶见细胞凋亡,结扎3d即见细胞凋亡增加,结扎7 d明显增加,结扎14 d后细胞凋亡达高峰,凋亡指数(AI)达58.2%±1.6%,各组AI有显著性差异(P＜0.05),21 d细胞凋亡数目明显减少.SABC免疫组化检测,Bcl-2蛋白的表达,对照组、胆总管结扎3 d,7 d均为阴性表达,14 d弱阳性表达,21 d强阳性表达;结扎14 d,Bcl-2蛋白弱阳性表达,AI达高峰,结扎21 d Bcl-2强阳性表达,AI下降.Bax蛋白的表达,对照组、胆总管结扎3 d均可见表达,7 d表达增多,14 d明显增多;21 d表达减少;结扎7 d,Bax蛋白中阳性表达,AI增高;结扎14 d,Bax蛋白强阳性表达,AI达高峰.表明在阻塞性黄疸过程中,Bcl-2蛋白表达越强,凋亡指数越少;Pax蛋白表达越强,凋亡指数越强.结论 Bcl-2和Bax蛋白均参与了阻塞性黄疸肝组织中细胞凋亡的调节,并在阻塞性黄疸肝损害的发生和发展中起重要作用.     

可复性梗阻性黄疸大鼠模型的建立与评价

目的:探究建立可复性梗阻性黄疸大鼠模型并评价临床实用价值.方法:"胆管结扎支撑管拔除法"建立可复性梗阻性黄疸大鼠模型.将Wistar大鼠32只,随机分为可复性梗阻性黄疸组(ROJ组)和梗阻性黄疸组(OJ组).ROJ组大鼠将胆总管与P I C C导管并行结扎致胆管梗阻,5 d后拔出PICC导管完成胆管再通,OJ组制成完全梗阻性黄疸模型.两组大鼠分别于术后5 d和8 d各处死8只,分别标记为ROJ5组、ROJ8组、OJ5组和OJ8组.每只大鼠于术前、术后第5天(拔管前)、第6天、第8天分别采血测定血总胆红素(total bilirubin,TBIL)、谷丙转氨酶(alanine aminotransferase,ALT)、碱性磷酸酶(alkaline phosphatase,ALP)水平,肠黏膜组织切片经HE染色,观察小肠黏膜形态学变化及损害情况.结果:ROJ5组与OJ5组相比,模型建立后5 d血TBIL、ALT和ALP变化规律相似,各时间点两者肝功能指标不存在差异,模型取出支撑管3 d后,血TBIL、ALT和ALP迅速恢复,肠黏膜损害也较前明显减轻;ROJ8组的肠黏膜损伤指数明显低于OJ8组,差异有统计学意义.结论:"胆管结扎支撑管拔除法"制作的可复性黄疸模型,是一种稳定可靠的可复性梗阻性黄疸大鼠模型.     

MRP2和NF-κB在阻塞性黄疸大鼠肝细胞中表达变化及意义

目的研究MRP2及NF—κB在阻塞性黄疸肝细胞中表达的变化,进一步阐明二者的关系。方法健康sD大鼠64只,将大鼠随机分为2组：假手术组（SHAM组）、胆总管结扎组（CBDL组）。建立大鼠阻塞性黄疸模型,SHAM组仅游离胆总管,不结扎离断胆总管。CBDL组予以结扎并切断胆总管。分别于术后的第3、7、14、21d各处死8只,用免疫组化法观察上述两组肝组织MRP2、NF—κBp65蛋白表达。结果SHAM组在第3、7、14、21dMRP2高水平表达,而NF—κBp65低水平表达。CBDL组大鼠NF—κBp65水平表达随着时间的延长而显著增高,MRP2低水平表达随着时间的延长而显著下降。结论阻塞性黄疸时,NF—κB的激活可能是引起MRP2表达下降的重要原因,NF—κB对MRP2调控可能起重要作用。     

胆管结扎和四氯化碳诱导Wistar大鼠肝纤维化模型的建立及相关指标的对比分析

目的比较胆管结扎(BDL)、四氯化碳(CCl4)诱导大鼠肝纤维化的生化指标、肝脏病理学及纤维连接蛋白(FN)的表达。方法 90只健康雄性Wistar大鼠,分为CCl4肝纤维化模型组(44只)及其对照组(6只)和BDL肝纤维化模型组(30只)及其对照组(10只)。CCl4肝纤维化模型组是采用50%的CCl4橄榄油溶液对大鼠进行腹腔注射的方法来制备模型,而BDL肝纤维化模型组则采用结扎大鼠胆总管的方法来制备。观察大鼠一般情况,生化方法测血清ALT、AST、TBil、DBil;ELISA法测血清透明质酸(HA)和层黏连蛋白(LN)水平。HE和Masson染色观察肝组织的病理学变化,免疫组织化学染色观察肝组织FN表达。计量资料组间比较采用t检验。结果血清生化学结果显示,BDL组大鼠自胆管结扎术后第7天开始,TBil及DBil即上升到较高水平且随后一直保持此水平,CCl4肝纤维化模型组大鼠2周始逐渐升高,至8周达高峰;BDL大鼠纤维化指标HA、LN水平显著高于同期CCl4模型组;CCl4模型组大鼠可见肝细胞弥漫性脂肪变性,汇管区-汇管区或汇管区-中央静脉间纤维间隔形成极为显著,BDL大鼠则表现为肝内胆管显著增生,炎性细胞浸润及纤维间隔形成同时存在;BDL组中FN的表达呈分散无规则型,且纤维组织细小,而CCl4组的FN多集中表达于小叶之间的间隔处,纤维组织粗大。结论 BDL和CCl4均可诱导大鼠肝纤维化,BDL较早引起肝功能及肝纤维化指标升高,可见明显胆管增生,CCl4则以脂肪变性为主;FN在两种模型中表达分布不同。     

七叶皂苷钠对博莱霉素致肺纤维化大鼠血清TNF-α的影响

50只Wistar雄性大鼠,随机分为空白对照组5只及盐水对照组、博莱霉素模型组、七叶皂苷钠(SA)治疗组各15只.采用一次性气管内注入博莱霉素A2诱导大鼠肺纤维化模型.SA治疗组造模后第2天给予SA(5 mg/kg)腹腔注射,模型组和盐水对照组给予等量的生理盐水腹腔注射,连续7 d.测定各组血清TNF-α的水平.结果模型组大鼠血清中的TNF-α水平较空白对照组、盐水对照组各时间点明显升高(P均＜0.01);SA治疗组各时间点血清中TNF-α水平较模型组明显降低(P＜0.01).早期应用SA干预治疗博莱霉素致肺纤维化大鼠可减缓其肺纤维化进程.     

L-精氨酸诱导实验性慢性胰腺炎大鼠模型的可行性分析

目的 初步探讨L-精氨酸诱导慢性胰腺炎大鼠动物模型的可行性.方法 将实验动物按完全随机法分为对照组及精氨酸12、24 h和7 d组,每组10只,间隔1 h分两次腹腔内注射L-精氨酸溶液造模.造模后相应时间点检测血淀粉酶、血糖水平,对胰腺组织进行病理评分,Van Gieson法对胰腺胶原纤维染色.结果 对照组及精氨酸12、24 h和7 d组的血淀粉酶水平分别为(1 634±890)U/L、(3 872±2 676)U/L、(3 307±2 197)U/L和(1 561±304)U/L,精氨酸7 d组血淀粉酶水平显著低于12 h和24 h组(P＜0.05),恢复到对照组水平.各组间血糖水平无明显差异.对照组及精氨酸12、24 h和7 d组胰腺的病理分值分别为0.8±0.4、5.1±2.6、6.5±2.2和4.5±1.6,精氨酸7 d组胰腺病理评分显著低于24 h组(P＜0.05),但仍显著高于对照组(P＜0.05).精氨酸7 d组胶原染色范围明显增加,其他各组未见明显胶原染色.结论 L-精氨酸腹腔注射后7 d可引起胰腺组织纤维化及管状复合结构增生,可用于探索慢性胰腺炎大鼠模型.     

姜黄素对腺嘌呤诱发的肾间质纤维化大鼠血及尿FN、TGF-β1、Col-Ⅳ水平的影响

目的 观察姜黄素对腺嘌呤诱发肾间质纤维化大鼠血、尿纤维连接蛋白（FN）、转化生长因子-β1（TGF-β1）、胶原蛋白-Ⅳ（Col-Ⅳ）水平的影响.方法 选择雄性Wistar大鼠84只,其中72只采用腺嘌呤混悬液连续灌胃制作腺嘌呤诱发RIF大鼠模型,将其中60只模型制作成功的大鼠随机分为5个组,分别为模型组、尿毒清组、姜黄素低剂量组、姜黄素中剂量组和姜黄素高剂量组各12只,另12只正常大鼠作为空白对照组.造模后24d姜黄素低、中、高剂量组大鼠分别给予125、250、500 mg/（kg·d）姜黄素灌胃;尿毒清组大鼠给予尿毒清颗粒3.75 g/（kg·d）灌胃;模型组与空白对照组大鼠给予等量蒸馏水灌胃,共处理60 d.采用双抗体夹心ELISA法检测大鼠血液及尿液中FN、TGF-β1、Col-Ⅳ水平.结果 模型组大鼠血、尿FN、TGF-β1、Col-Ⅳ高于空白对照组（P均＜0.05）,姜黄素各剂量组各指标有所下降,以高剂量组效果最佳,尿毒清组各指标也有所下降,但高于姜黄素高剂量组.结论 姜黄素可能通过下调肾间质纤维化大鼠血、尿FN、TGF-β1、Col-Ⅳ水平干预肾间质纤维化,效果优于尿毒清.     

类似人类老年糖尿病大鼠模型之形态学变化

目的 采用D-半乳糖加高脂高糖乳剂及链脲佐菌素(STZ)构建类似老年人糖尿病的大鼠动物模型,观察其胰腺形态学变化.方法 选用健康Wistar雌性大鼠,20只灌胃生理盐水为正常对照组;20只采用腹腔注射D-半乳糖40 d为衰老模型组;另25只则采用腹腔注射D-半乳糖40 d并灌胃高脂高糖乳剂30 d后腹腔注射STZ(体重≤200 g按30 mg/kg,体重＞200 g者按体表面积进行计算),制备衰老糖尿病模型大鼠,筛选空腹血糖≥11.1 mmol/L者为成模鼠,上述各组大鼠再继续灌胃生理盐水10 d后,各组随机取10个样本以免疫组化、光镜和电镜分别观察大鼠胰岛诱导型一氧化氮合酶(iNOS)表达、胰腺细胞凋亡、胰岛形态及胰岛细胞和腺泡细胞超微结构变化.结果 衰老模型组大鼠胰岛iNOS表达量和胰腺细胞凋亡数较正常对照组增加,衰老糖尿病模型组胰岛iNOS表达量和胰腺细胞凋亡数剧增达3倍以上.HE染色显示,衰老模型组胰岛数量、面积仅为正常的50%～70%,衰老糖尿病模型组胰岛数量、面积仅为正常的20%～30%,且岛内中心部细胞(β细胞)消失尤为显著.电镜观察显示,衰老糖尿病模型组大鼠胰腺细胞明显脱颗粒,呈现膜性结构皱缩,核染色质固缩、碎裂等细胞凋亡征象.结论 采用腹腔注射D-半乳糖加高脂高糖乳剂及腹腔注射STZ,胰腺形态组织学证实大鼠在衰老模型基础上胰岛β、D细胞数量进一步下降可引发糖尿病.     

Pressure measurements from biliary and pancreatic segments of sphincter of oddi

Using a minimally compliant infusion system and a triple-lumen pressure recording catheter, we obtained endoscopic manometric measurements from both the common bile duct and pancreatic duct segments of the sphincter of Oddi (SO) in 58 patients. Fifteen patients (ages 27–69) had the diagnosis of functional abdominal pain, 19 patients (ages 30–76) had partial biliary obstruction, and 24 patients (ages 15–80) had idiopathic acute recurrent pancreatitis. Resting ductal pressure was similar in the common bile duct and pancreatic duct in all patient groups. In the group with functional pain, basal SO pressure was similar, whether obtained from the common bile duct or pancreatic duct sphincteric segment. Eight of 19 patients with partial biliary obstruction had elevated basal SO pressure. Five of these eight patients had elevated basal SO pressure confined exclusively to the common bile duct segment of the sphincter, while three patients had elevated basal SO in both segments. Conversely seven of 24 patients with acute recurrent pancreatitis had an elevated basal SO pressure, with five patients having pressure elevation only in the pancreatic duct segment while two patients had abnormal basal SO pressure in both segments. We conclude that selective cannulation of the common bile duct and/or the pancreatic duct during manometric study of the SO is necessary in order to diagnose segmental SO dysfunction responsible for partial biliary obstruction or episodes of acute recurrent pancreatitis.     

急性胆源性胰腺炎早期内镜治疗价值

目的探讨急性胆源性胰腺炎早期内镜治疗的价值及其安全性。方法选择92例急性胆源性胰腺炎患者早期（72h内）行ERCP及内镜治疗（ERCP组），并与同期保守治疗40例（对照组）进行比较。结果ERCP组全部成功实施十二指肠乳头切开取石，72例胆总管结石者行网篮及气囊取石，所有92例均行鼻胆管引流，重症组10例同时行胰管支架引流。ERCP组平均腹痛消失时间、血清淀粉酶恢复时间、平均住院天数及平均费用均明显低于对照组。ERCP组重症组病死率8．3％，对照组重症组病死率33．3％。结论急性胆源性胰腺炎早期ERCP治疗是安全的，能降低患者的病死率，减少患者住院天数和费用。     

Histological alterations of the preampullary common bile and pancreatic duct in acute biliary and nonbiliary pancreatitis

Histological alterations of the preampullary common bile duct and the pancreatic duct were studied in the pancreata from 16 patients with acute biliary pancreatitis and 11 patients with acute nonbiliary pancreatitis. The corresponding controls either suffered from gallstone disease without pancreatitis or had neither gallstone disease nor pancreatitis. In acute biliary pancreatitis as well as in gallstone disease, a common channel is significantly less frequent than in acute nonbiliary pancreatitis and in the normal pancreas. The inflammatory alterations of the preampullary common bile duct are increased in biliary pancreatitis compared to nonbiliary pancreatitis and to controls. The inflammatory lesions of the distal common bile duct and distal pancreatic duct are significantly correlated. These findings favor the assumption that acute biliary pancreatitis is initiated by transient obstruction of the preampullary common bile duct producing a local inflammation which encroaches upon the adjacent region of the pancreatic duct.     

Complete obstruction of the lower common bile duct caused by autoimmune pancreatitis: is biliary reconstruction really necessary?

Recent observations suggest that an immune response is involved in the development of chronic pancreatitis. We report a case of autoimmune pancreatitis in a patient who showed complete obstruction of the lower common bile duct. A 63‐year‐old man was admitted to a local hospital, complaining of appetite loss and back pain. The patient had obstructive jaundice, and percutaneous transhepatic gallbladder drainage was performed. Fluorography through the biliary drainage catheter showed complete obstruction of the lower common bile duct. The patient had no history of alcohol consumption and no family history of pancreatic disease. Physical examination revealed an elastic hard mass palpable in the upper abdomen. Abdominal ultrasound and abdominal computed tomography (CT) scans showed enlargement of the pancreas head. While autoimmune pancreatitis was highly likely, due to the patient's high serum immunoglobulin level, the possibility of carcinoma of the pancreas and/or lower common bile duct could not be ruled out. Laparotomy was performed, and wedge biopsy samples from the pancreas head and body revealed severe chronic pancreatitis with infiltration of reactive lymphocytes, a finding which was compatible with autoimmune pancreatitis. Cholecystectomy and biliary reconstruction, using choledochojejunostomy, were performed, because the complete bile duct obstruction was considered to be irreversible, due to severe fibrosis. After the operation, prednisolone (30 mg/day) was given orally for 1 month, and the entire pancreas regressed to a normal size. Complete obstruction of the common bile duct caused by autoimmune pancreatitis has not been reported previously; this phenomenon provides an insight into autoimmune pancreatitis and provokes a controversy regarding whether biliary reconstruction is needed for the treatment of complete biliary obstruction caused by autoimmune pancreatitis.     

Chronic Pancreatitis and the Hepatobiliary System

Alcohol-induced chronic pancreatitis involving the head of pancreas may have profound effects on the hepatobiliary system. The natural history, complications, and management of the syndrome are presented, using selected cases to emphasize important features. Chronic pancreatitis can cause mechanical obstruction to both the distal common bile duct and the proximal pancreatic duct. In the common bile duct this will result in proximal dilatation above the stenosis with bile stasis. Possible sequelae are ascending cholangitis, cholecystitis, biliary calculi formation, and secondary biliary cirrhosis. The mechanical effects of stricture of the proximal pancreatic duct may exacerbate pancreatic dysfunction. The clinicopathological spectrum of chronic pancreatitis with biliary obstruction encompasses three clinical types–"transient,""recurrent." and "persistent." The widespread effects of the syndrome are evident from the involvement of pancreas, proximal pancreatic duct, papilla of Vater, liver, peripheral biliary tree, common bile duct, gallbladder, and reticuloendothelial system. Essential to management is surgery which should be considered when there is objective evidence of obstruction to the common bile duct. Choledochoduodenostomy is the preferred type of operation. If dilatation is mild and jaundice transient, conservative therapy with careful observation is advocated.     

一氧化氮合酶在急性胰腺炎大鼠胰岛中的表达

在SD大鼠以胰胆管结扎法建立急性胰腺炎模型，在急性胰腺炎大鼠胰岛β细胞神经元型一氧化氮合酶(nNOs)表达和血清一氧化氮(N0)水平下降，血清葡萄糖和淀粉酶水平升高，提示急性胰腺炎时内分泌紊乱可能与胰岛β细胞nNOS表达下调有关。     

Biochemical and morphological changes that characterise recovery from necrotising biliary pancreatitis in the opossum.

The events that characterise recovery from severe biliary pancreatitis have not been defined. This study used a reversible model of necrotising pancreatitis, induced by obstructing the opossum common bile pancreatic duct (CBPD), to evaluate this phenomenon. The CBPD of opossums was obstructed with a balloon tipped catheter for five days and then decompressed by removal of the catheter. Recovery was evaluated 0-90 days after relief of obstruction. Serum bilirubin and amylase values rapidly declined, reaching control values 7-14 days after removal of the obstructing catheter. Pancreatic protein and amylase values were transiently increased shortly after relief of obstruction but returned to control values 21 days after decompression. Pancreatic ornithine decarboxylase activity and incorporation of [3H]-thymidine into DNA were transiently increased 14 days after duct decompression suggesting that regeneration occurs at approximately that time. Foci of pancreatic necrosis involved roughly 40% of the gland at time of decompression but these foci gradually disappeared and the gland resembled that of control animals 60 days after decompression. Evidence of fibrosis or collagen deposition in the pancreas was not noted at any time. These studies show that recovery after necrotising biliary pancreatitis occurs comparatively rapidly and the restitution ad integrum occurs. Recovery from necrotising acute pancreatitis in this model is not associated with the development of chronic pancreatitis.     

Clinical significance of manometric assessment of both pancreatic duct and bile duct sphincter in the same patient

In this study both pancreatic and bile duct sphincter pressures were measured on the same occasion by means of endoscopic manometry in 42 patients with long-standing upper abdominal pain. Nine (53%) of the 17 patients with abnormal sphincter function had a marked difference between the pancreatic duct sphincter pressure (PSOP) and the bile duct sphincter pressure (BSOP): 6 patients with a clinical diagnosis of biliary dyskinesia showed elevated BSOPs, whereas the PSOPs were normal. The reverse, an abnormal PSOP but normal or only a slightly elevated BSOP, was registered in the three patients with chronic pancreatitis. These findings indicate that a motor abnormality may be restricted to only one of the sphincters. Thus, when the sphincter of Oddi is investigated only from the pancreatic duct, manometry may either fail to show an abnormal BSOP in some patients with biliary dyskinesia, or it may falsely suggest this diagnosis in patients with unrecognized pancreatitis.     

Endoscopic therapy for chronic pancreatitis: An evidence-based review

In the setting of chronic pancreatitis, pancreatic ductal obstruction, and ductal leak, pseudocyst formation and biliary obstruction present many challenges for endoscopists. Although chronic pancreatitis has a variety of clinical manifestations, most commonly patients present with intermittent or chronic abdominal pain. Recent studies suggest stenting of pancreatic ductal strictures has a significant impact on reducing chronic pain. The removal of ductal calculi, presumably from relieving obstruction, also improves abdominal pain. When the site of leak is bypassed, ductal leaks may be cured by endoscopic stenting. Multiple plastic bile duct stents to treat chronic pancreatitis-associated bile duct stricture can delay the need for surgery. Although these endoscopic techniques have been beneficial for many patients, further study is warranted to better define their role in chronic pancreatitis compared with well-established surgical techniques.     

PROPHYLACTIC PANCREAS STENTING FOLLOWED BY NEEDLE‐KNIFE FISTULOTOMY IN PATIENTS WITH SPHINCTER OF ODDI DYSFUNCTION AND DIFFICULT CANNULATION: NEW METHOD TO PREVENT POST‐ERCP PANCREATITIS

Introduction: The aim of the present study was to reduce post‐endoscopic retrograde cholangiopancreatography (ERCP) complications with a combination of early needle‐knife access fistulotomy and prophylactic pancreatic stenting in selected high‐risk sphincter of Oddi dysfunction (SOD) patients with difficult cannulation. Methods: Prophylactic pancreatic stent insertion was attempted in 22 consecutive patients with definite SOD and difficult cannulation. After 10 min of failed selective common bile duct cannulation, but repeated (>5×) pancreatic duct contrast filling, a prophylactic small calibre (3–5 Fr) pancreatic stent was inserted, followed by fistulotomy with a standard needle‐knife, then a standard complete biliary sphincterotomy followed. The success and complication rates were compared retrospectively with a cohort of 35 patients, in which we persisted with the application of standard methods of cannulation without pre‐cutting methods. Results: Prophylactic pancreatic stenting followed by needle‐knife fistulotomy was successfully carried out in all 22 consecutive patients, and selective biliary cannulation and complete endoscopic sphincterotomy were achieved in all but two cases. In this group, not a single case of post‐ERCP pancreatitis was observed, in contrast with a control group of three mild, 10 moderate and two severe post‐ERCP pancreatitis cases. The frequency of post‐ERCP pancreatitis was significantly different: 0% versus 43%, as were the post‐procedure (24 h mean) amylase levels: 206 U/L versus 1959 U/L, respectively. Conclusions: In selected, high‐risk, SOD patients, early, prophylactic pancreas stent insertion followed by needle‐knife fistulotomy seems a safe and effective procedure with no or only minimal risk of post‐ERCP pancreatitis. However, prospective, randomized studies are awaited to lend to support to our approach.