FK506对急性坏死性胰腺炎大鼠肺损伤的保护作用

目的 :实验观察FK5 0 6对大鼠胰腺炎肺损伤的保护作用。方法 :牛磺胆酸钠胰胆管逆行注入法诱导大鼠急性胰腺炎模型。SD大鼠随机分为 3组 :对照组实验前 12h及 1h分别以生理盐水(4mL kg)灌胃 ,实验时经胰胆管逆行注入生理盐水 ;胰腺炎组实验时经胰胆管逆行注入 5 %牛磺胆酸钠(80mg kg) ;FK组实验前 12h及 1h分别以FK5 0 6 (4mL kg)灌胃。观察 2 4h存活率 ,血清TNF α水平 ,肺湿重 干重比值和肺组织病理切片的变化。结果 :胰腺炎组 2 4h大鼠存活率 5 0 % ,FK组 10 0 % ,FK组肺湿重 干重比值和显微镜下病理损伤程度较未预防组明显减轻 ,血清TNF α水平也降低。结论 :FK5 0 6对急性坏死性胰腺炎导致的肺损伤具有明显的保护作用 ,其机理可能是通过抑制TNF α等炎性细胞因子的释放减轻了肺损伤     

光子照射治疗痔疮手术后创面愈合的效果观察

目的 探讨光子照射治疗痔疮手术后创面愈合的效果.方法 选择将80例痔疮手术后患者,随机分为观察组、对照组各40例.对照组给予预防性抗感染、止血、换药处理等,观察组在对照组基础上,每日加用光子照射手术创面.观察两组术后4、6、8d创面疼痛程度、创面渗液情况及创面愈合时间.结果 与对照组比较,观察组疼痛程度、创面渗液情况、创面愈合时间与对照组的相比,创面疼痛程度、创面渗液情况明显缓解(P均＜0.05),愈合时间明显缩短(P＜0.05).结论 光子照射治疗痔疮术后创面简单易行,能减轻患者痛苦,减轻创面渗液症状,促进术后创面愈合,值得推广应用.     

盐酸戊乙奎醚对大鼠急性坏死性胰腺炎肺损伤MIF和AQP-5表达的影响

目的:探讨盐酸戊乙奎醚对大鼠急性坏死性胰腺炎(acute necrotic pancreatitis,ANP)并发急性肺损伤(acute lung injury,ALI)血清巨噬细胞移动抑制因子(macrophage migration inhibitory factor,MIF)和肺泡灌洗液水通道蛋白-5(aquaporin-5,AQP-5)表达的影响.方法:采用经胰胆管内逆行注射4%牛磺胆酸钠构建大鼠ANP并发ALI模型,100只SD大鼠以是否接受盐酸戊乙奎醚(penehyclidine hydrochloride,PHCD)腹腔注射干预治疗随机分为治疗组和非治疗组,每组再以6h、12h、24h、36h、48h五个取材时间点继续随机分组,共10组,每组10只动物.采用ELISA法测定血清中MIF的浓度和肺泡灌洗液中AQP-5的浓度,同时进行胰腺和肺组织病理形态学观察,肺组织湿/干重比检测,动脉血气分析.结果:相同时间点PHCD治疗组与非治疗组比较显示,血清MIF浓度降低(χ2=20.52,P=0.042),肺泡灌洗液AQ P-5浓度增高(χ2=17.22,P=0.044),胰腺和肺组织病理学损伤减轻,肺组...     

不同剂量重组人生长激素对2型糖尿病大鼠创面愈合的影响

目的探讨重组人生长激素(rhGH)对T2DM大鼠创面愈合的影响。方法建立T2DM大鼠创面模型,32只大鼠随机分为对照组(T2DM)、rhGH 0.2 IU/kg组(rhGH 0.2)、rhGH0.4 IU/kg组(rhGH 0.4)、rhGH 0.6 IU/kg组(rhGH 0.6),每组8只,各组分别予0.9%生理盐水和0.2、0.4、0.6 IU/kg rhGH干预14 d。观察各组第0、3、7、14天时平均残余创面面积及创面完全愈合时间,检测干预前后血糖水平,HE染色观察创面组织病理变化。结果 14 d时,rhGH 0.2、rhGH 0.4、rhGH 0.6组残余创面面积小于T2DM组(P<0.05),rhGH 0.2、rhGH 0.4、rhGH 0.6组残余创面面积依次减小(P<0.05),rhGH 0.4、rhGH 0.6组平均创面完全愈合时间短于T2DM、rhGH 0.2组(P<0.05)。各组血糖趋势随时间递增,各组间相同时间点血糖水平比较差异无统计学意义(P>0.05)。HE染色结果显示,T2DM、rhGH 0.2组创面组织内炎性细胞浸润较多;rhGH 0.4、rhGH 0.6组上皮化水平及胶原形成较好,创面愈合程度高。结论 0.6 IU/kg剂量rhGH能缩短T2DM大鼠创面慢性炎症浸润时间,加速创面愈合速度,予小剂量rhGH治疗DM创面时,不会引起血糖明显升高。     

白竭散治疗肛周脓肿合并糖尿病术后创面24例效果观察

目的分析白竭散治疗肛周脓肿合并糖尿病术后创面效果。方法选取从2015年1月—2016年1月收治的24例肛周脓肿合并糖尿病患者,随机分为对照组(12例)与观察组(12例),对照组术后使用凡士林纱布换药,观察组术后使用白竭散换药,对比两组创面疼痛评分、创面渗液评分、创面愈合率、成纤维细胞数量。结果观察组成纤维细胞数量、创面愈合率明显优于对照组(P0.05)。观察组渗液评分、创面疼痛评分低于对照组(P0.05)。结论肛周脓肿合并糖尿病患者,术后创面使用白竭散治疗,能减少渗液,缓解疼痛,促进创面愈合。     

环氧合酶-2抑制剂对大鼠胃黏膜损伤愈合的影响

目的　环氧合酶 (COX)是合成前列腺素 (PGs)的关键酶 ,传统的非甾体抗炎药 (NSAIDs)抑制COX 1和COX 2活性 ,引起严重的胃肠道不良反应。特异性COX 2抑制剂有望成为不引起胃损伤的新型NSAIDs。本研究探讨特异性和非特异性COX 2抑制剂对盐酸诱导大鼠胃黏膜损伤愈合的影响。方法　雄性SD大鼠胃内给予 0 .6mol/LHCl1ml,Westernblot和免疫组化法分析胃黏膜COX 1和COX 2表达。盐酸灌胃后 10min ,实验组胃内给予NS 3980 .4、4、4 0mg/kg和吲哚美辛 4 0mg/kg ,对照组胃内给予 1%阿拉伯树胶 (AG) 5ml/kg。盐酸灌胃前和灌胃后 1、3、6、12、2 4及 4 8h分别处死大鼠 ,剖腹取胃 ,观察各组动物损伤指数 (LI)及光镜下的胃黏膜病理学改变。结果　盐酸灌胃后COX 2在表层上皮细胞和颈黏液细胞表达显著增加 ,NS 398和吲哚美辛均延迟胃黏膜损伤的愈合。盐酸灌胃后 12h ,NS 398组 (4和 4 0mg/kg)及吲哚美辛组的LI分别为 (1.4 2± 0 .2 3) % ,(1.4 2± 0 .2 9) %和 (1.6 2± 0 .4 4 ) % ,明显高于对照组的 (0 .5 8± 0 .2 4 ) % (P <0 .0 5 )。结论　特异性和非特异性COX 2抑制剂延迟大鼠胃损伤后的愈合 ,提示COX 2表达在胃黏膜再生过程中起重要作用     

低剂量辐射通过诱导局部SDF1/CXCR4高表达促进大鼠糖尿病皮肤损伤愈合

目的探讨低剂量辐射促进糖尿病(DM)皮肤损伤愈合的分子机制,明确SDF1、CXCR4在创面愈合过程中的作用。方法制备DM皮肤损伤大鼠模型,分为2组,其中照射组(RDM组)给予75 m Gy的X射线照射,6 min·次~(-1)·d~(-1),照射5 d,间隔2 d,总共照射15 d。另一组为DM大鼠非照射组(DM)组;同时以正常大鼠皮肤损伤自然愈合为对照组(NDM组)。分别在创面愈合的7、14、21 d,通过创面愈合面积、免疫组化和蛋白印记方法观察低剂量辐射对DM皮肤损伤创面愈合的影响,确定辐照对皮肤创面组织表达SDF1/CXCR4的调节作用。结果 DM大鼠创面存在难以愈合及愈合延迟的现象。RDM组大鼠的创面愈合率明显高于未照射组(P0.01);免疫组化结果显示DM组创面边缘的SDF1和CXCR4蛋白表达明显低于正常大鼠(P0.01),RDM组SDF1和CXCR4蛋白与DM组相比增加(P0.01);采用蛋白印记方法分析创面愈合过程SDF1/CXCR4的动态表达,结果显示RDM组7 d SDF1表达与DM组相比增加2.8倍。关联分析发现,SDF1表达强度与创面微血管密度密切相关。结论低剂量辐射参与创面修复整个过程,通过诱导DM皮肤创面局部组织分泌大量的SDF1,招募外周血中EPCs,促进局部新生血管生成,加速创面愈合。     

川芎嗪对急性坏死性胰腺炎大鼠胰腺及肾损伤的保护作用

目的 探讨川芎嗪对急性坏死性胰腺炎（ANP）胰腺及肾损伤的保护作用。方法 192只SD大鼠,随机分为对照（C）组、胰腺炎（P）组、川芎嗪治疗（T）组,并制作模型。三组模型制作后0．5、2、6及12h分别测定肾血流量,对胰腺、肾组织病理进行评分、分级,观察肾功能及血栓素A2（TXA2）／前列环素（PGI2）。结果 与C组相比,P组各时间点肾血流量均明显降低（P〈0．01）,胰腺及肾病理改变明显加重,血浆尿素氮（BUN）、肌酐（Cr）明显升高（P均〈20．05）,TXA2／PGI2在2、6、12h明显增加（P〈0．01）。与P组相比,T组各时间点肾血流量均明显增加（P〈0．01）,胰脓及肾的病理损害有所减轻．血浆BUN、Cr较C组明显降低（P均〈0．05）,TXA2／PGI2在6、12h明显降低（P均〈0．05）。结论 川芎嗪可以减轻ANP大鼠的胰腺及肾损伤。     

氯胺酮在中、高位硬膜外阻滞麻醉中的应用

目的探讨硬膜外腔注入阈剂量氯胺酮在中、高位硬膜外阻滞麻醉中的作用。方法 90例患者随机分为三组,每组30例。三组均注入常规试验量,A组注入常规液5~10 ml;B组注入常规液＋0.1%肾上腺素0.1 ml 5~10 ml;C组先注入0.3 mg/kg的氯胺酮稀释液5 ml,再注入常规液5~10 ml。观察患者的呼吸循环变化,术后镇痛时间及效果。结果与麻醉前相比C组循环稳定,MAP、HR A组比B组下降明显（P〈0.05）;记录术后2~6 h各时点患者疼痛VAS〈5的例数,与A组对比得出：C组镇痛时间和效果明显优于B组、A组。结论硬膜外腔注入阈剂量氯胺酮可对抗硬膜外阻滞所致的血压下降、心率减慢;还可发挥超前镇痛作用。     

糖皮质激素对急性胰腺炎大鼠胰腺细胞凋亡的影响及其意义

目的　探讨糖皮质激素对急性胰腺炎 (AP)大鼠胰腺细胞凋亡的影响及其意义。方法　将SD大鼠 5 4只随机分为 3组 :正常对照组 ,胰腺炎组和激素治疗组 ,每组 18只。经十二指肠行胆胰管逆行加压注射 4 %的牛磺胆酸钠 ,诱导大鼠 AP模型 ,于术后 3h、6 h和 12 h采取断颈方法分批处死动物 ,应用末端脱氧核苷酸转换酶 (Td T)介导的原位末端标记 (TUNEL )法检测胰腺组织细胞凋亡变化 ,观察各组大鼠胰腺组织病理改变。结果　 (1) AP大鼠的胰腺凋亡细胞增多 ,与对照组比较均有显著差异 (P<0 .0 1) ,注射激素后 ,胰腺凋亡细胞减少 ,6 h、12 h的凋亡指数均显著低于对应时相的 AP组 (P<0 .0 5 ) ;(2 )激素治疗后 ,AP大鼠胰腺炎症细胞、坏死细胞明显减少 ,病变减轻 ,6 h、12 h病理评分均显著低于 AP组 (P<0 .0 5 )。结论　糖皮质激素具有抑制胰腺细胞凋亡的作用 ,保护腺泡细胞、阻止细胞死亡可能是糖皮质激素减轻 AP病变严重程度的一个重要因素。     

胰腺残端缝合方式预防胰腺远端切除术后胰漏的动物实验

[目的]探讨不同胰腺残端缝合方式预防胰腺远端切除术后胰漏的效果.[方法]将34只实验用猪随机分为研究组与对照组,每组17只.研究组:超声刀横断胰腺,用4-0 Prolene线间断缝合胰腺残端,主胰管单独结扎;对照组:超声刀横断胰腺,用4-0 Prolene线U形交锁缝合胰腺残端,主胰管单独结扎.观察2组术后的胰漏情况,...     

Protective effect of misoprostol, a synthetic prostaglandin E1 analog, on experimental pancreatitis induced by pancreatic duct ligation in rat

This study was performed to assess the effects of misoprostol (M), a synthetic prostaglandin E1 analog, on experimental pancreatitis in rat. Pancreatitis was induced by ligation of the main pancreatic duct of 3-month-old male Wistar rats. Pancreatic lesions were observed at 6, 12, 24, 48, and 96 h after pancreatic duct ligation (PDL). A time of 48 h was chosen to evaluate M treatment. M was injected intraperitoneally (500 micrograms/kg every 4 h) between time 0 and 48 h after PDL. Stereological analysis was performed on light and electron microscopy. Total pancreatic amylase and chymotrypsin concentrations were determined. Four groups of five rats were studied: sham operated (SO), M without PDL (PG), duct ligation without M (DL), and duct ligation with M (DLPG). Edema, dedifferentiation of pancreatic acinar cells, and heterogeneous distribution of zymogen granule diameters observed after PDL were significantly decreased by M in the DLPG group. Enzyme concentrations were also decreased by M in the DLPG group. Enzyme concentrations were also decreased by M both in normal (PG) and duct ligated rats (DL). M has protective effects against pancreatic lesions induced by PDL. In this model, the protective effect of M may be due to a blockade of the autodigestive secretions of the pancreatic acinar cells.     

还原性谷胱甘肽对重症急性胰腺炎大鼠早期胰肝损伤的保护作用

目的阐明还原性谷胱甘肽对重症急性胰腺炎早期胰肝损害的保护作用。方法 54只雄性Wistar大鼠随机分三组,每组18只:A组为正常对照组,开腹后仅翻动胰腺,即关腹;B组为重症急性胰腺炎(SAP)组,以0.1 mL/min的速度向胰胆管内逆行注入4.5%牛磺胆酸钠(1 mL/kg)建立大鼠SAP模型;C组为N-乙酰半胱氨酸(NAC)处理组,术前0.5 h,用NAC(200 mg/kg)腹腔注射,接着建立大鼠SAP模型。于造模术后6 h,麻醉大鼠获取新鲜胰腺和肝脏组织,取一部分用于GSH检测,另一部分用于病理学观察和电镜观察。结果胰腺组织中还原性谷胱甘肽(GSH)水平为:对照组>NAC处理组>SAP组,差异有统计学意义(P<0.05)。胰腺组织病理学检查及评分:SAP组和NAC处理组大鼠出现急性坏死性胰腺炎病变,但NAC处理组胰腺组织坏死比SAP组胰腺组织坏死程度减轻。SAP与NAC处理组比较差异有统计学意义(P=0.0368,P<0.05)。6 h电镜观察:N-乙酰半胱氨酸能改善胰腺腺泡细胞内酶原颗粒运转,肝脏超微结构显示,SAP组内质网扩张,线粒体肿胀,NAC处理组局部可见内质网扩张。结论随着GSH的消耗,发病早期(6 h)就可以出现胰肝损害,补充N-乙酰半胱氨酸能减轻胰腺和肝脏的损害。     

乌司他定对急性坏死性胰腺炎大鼠合并肺损伤的影响

目的 探讨乌司他定(UT1)对急性坏死性胰腺炎大鼠(ANP)合并肺损伤时肺内ET-1和NF-κB表达及肺损伤的影响.方法 60只SD大鼠按随机数字法分成假手术组、ANP组和UTI组,各20只.采用胆胰管逆行注射5%牛磺胆酸钠溶液1 ml/kg体重制备ANP模型,假手术组胰管注射等量生理盐水,UT1组在ANP制模成功后即从大鼠尾静脉注射UTI 10 000 U/kg体重.24 h后处死动物,测血清淀粉酶、TNF-α、肺组织湿/干重比,免疫组化法检测肺组织NF-κB和ET-1蛋白表达以及使用TUNEL法检测细胞凋亡.结果 UTI组术后24 h血清淀粉酶、TNF-α和肺湿/干重比分别为(5 648±378)U/L、(89.19±3.54)ng/L和4.55±0.07,较ANP组的(6 799±437)U/L、(183.30±8.18)ng/L和4.89±0.20显著降低(P＜0.05).假手术组末见NF-κB和ET-1表达,未见凋亡细胞.UTI组NF-κB和ET-1阳性表达率分别为(19±3)%和(8±1)%,较ANP组的(25±2)%和(13±1)%显著降低(P＜0.05).UTI组细胞凋亡指数为13.75±1.25,较ANP组的6.90±0.85显著升高(P＜0.05).结论 ANP时肺组织NF-κB和ET-1的高表达可能导致肺损伤.UTI能改善肺微循环,减轻肺炎症性损伤.     

Thymosin alpha 1 improves severe acute pancreatitis in rats via regulation of peripheral T cell number and cytokine serum level

AIM: The aim of this study was to investigate the effect of thymosin alpha 1 (TA1) on severe acute pancreatitis (SAP) in rats. METHODS: Healthy Sprague-Dawley rats (n = 72) were randomly divided into four groups: control group, SAP group, and two TA1 treated groups. SAP was induced by injection of 5% sterile sodium taurocholate into the biliopancreatic duct (BPD), after which TA1 was given subcutaneously at 0 and 2 h at a dose of 100 microg/kg. The rats were killed at 3, 6 and 12 h, respectively. Serum amylase and lipase, interleukin (IL)-1beta, tumor necrosis factor-alpha (TNF-alpha), pancreatic wet/dry weight ratio and the percentage of CD3/CD4+/CD8+ T cells in peripheral blood mononuclear cells (PBMC) were measured. Next, 30 rats were randomly divided into three groups (each group containing 10 animals): SAP group (S) and two TA1 treated groups. The effects of TA1 on the survival of SAP were assessed 72 h after the induction of SAP. RESULTS: There was no significant change in the serum amylase and lipase levels after TA1 administration. Levels of serum IL-1beta, TNF-alpha and pancreatic wet/dry weight ratio were significantly reduced after TA1-treatment. Application of TA1 significantly balanced CD3/CD4+/CD8+ T cells of PBMC and improved histological scores and the survival rate. CONCLUSION: TA1 can reduce pancreatic inflammation by regulating differentiation of CD3/CD4+ T cells and decreasing the release of cytokines, thus attenuates pancreatic severity in SAP rats.     

Effects of the use of fibrin glue around the colonic anastomosis of the rat

Abstract. Background: This study was aimed at examining whether the addition of fibrin glue to a sutured colonic anastomosis improves its healing or not. Methods: We studied the effect of adding fibrin glue on a sutured colonic anastomosis. Thirty-six Wistar rats were randomized into two groups of 18 rats each. A sutured anastomosis was performed in all rats. Fibrin glue was applied around the anastomosis of the rats of group B. Rats were sacrificed on the eighth postoperative day. Results: The rate of anastomotic leakage was found not to be significantly different between the two groups. The mean bursting pressure of the colonic anastomoses was significantly higher in group B (fibrin-treated) than in group A. Conclusion: Fibrin glue application around a sutured anastomosis provides a safer anastomosis which is stronger than the sutured one.     

Ductal Factors in the Pathogenesis of Acute Pancreatitis in the Rat

In 66 male rats the hepatic duct was ligated close to the duodenum creating obstruction of both bile and pancreatic outflow, in another 60 rats the hepatic duct was ligated close to the duodenum, but the bile flow shunted from the proximal part of the hepatic duct to the duodenum, creating an isolated obstruction of the pancreatic outflow. In the first group, when the bile flow was stimulated with cholecystokinin (Cecekin®), reflux of bile into the pancreas occurred, resulting in a high frequency of hemorrhagic pancreatic necrosis. Reflux of bile did not occur and pancreatic necrosis was infrequent after secretin administration or in controls without stimulation, in the second group pancreatic necrosis occurred infrequently. From these experiments the following conclusions may be drawn: 1. In hepatic duct obstruction, when a common channel mechanism is present, reflux of bile into the pancreas occurs, if the bile flow is increased, 2. Reflux of bile causes severe damage to the pancreas, 3. Simple obstruction of the pancreatic outflow most often results in edematous pancreatitis and infrequently in pancreatic necrosis. The frequency of necrosis is not altered if the pancreatic secretion is stimulated with pancreozymin or secretin.     

Endoscopic manometry of the sphincter of Oddi and pancreatic duct in chronic pancreatitis

Pancreatic duct pressure was studied by endoscopic manometry in 12 patients with chronic pancreatitis and in 9 patients with a normal pancreas (suspected biliary dyskinesia). To study the effect of increased intraduodenal concentration of pancreatic enzymes, the duct pressure was measured before and after intraduodenal enzyme infusion. The mean pancreatic duct pressure was 12 (range, 6-25) mm Hg and 18 (range, 6-38) mm Hg in the pancreatitis and 'control' groups, respectively. The occasional patient in each group who had a high duct pressure also had an elevated sphincter of Oddi pressure. A significant correlation between the two pressures was found in both groups of patients. During intraduodenal infusion of pancreatic enzymes a decrease of the pancreatic duct pressure occurred in only two patients. We conclude that an increased pancreatic duct pressure is not a frequent finding in chronic pancreatitis. An elevation of the duct pressure can also be found in patients without pancreatitis. The sphincter of Oddi pressure appears to be more important for the pancreatic duct pressure than the severity of the pancreatitis. Intraduodenal infusion of enzymes, as done in our study, had an inconsistent effect on the pancreatic duct pressure.     

Promoting Diabetic Wound Therapy Using Biodegradable rhPDGF-Loaded Nanofibrous Membranes: CONSORT-Compliant Article

The nanofibrous biodegradable drug-loaded membranes that sustainably released recombinant human platelet-derived growth factor (rhPDGF-BB) to repair diabetic wounds were developed in this work.rhPDGF-BB and poly(lactic-co-glycolic acid) (PLGA) were mixed in hexafluoroisopropyl alcohol, followed by the electrospinning of the solutions into biodegradable membranes to equip the nanofibrous membranes. An elution technique and an enzyme-linked immunosorbent assay kit were used to determine the rhPDGF-BB release rates in vitro and in vivo from this membrane. Eighteen Sprague-Dawley streptozotocin-induced diabetic rats were randomized into 3 groups: rhPDGF-BB-loaded nanofibrous membrane group, PLGA only membrane group, and conventional gauze sponge group for the wound associated with diabetes of rat in each group.The nanofibrous biodegradable membranes released effective concentrations of rhPDGF-BB for over 21 days. The nanofibrous rhPDGF-BB-loaded PLGA membranes contained more water and were further hydrophilic than PLGA only fibers. The rhPDGF-BB-loaded PLGA membranes considerably helped the diabetic wounds repairing. Furthermore, the proliferative cells and angiogenesis of rats associated with diabetes by rhPDGF-BB-loaded nanofibrous membranes were greater than those of other groups, owing to the increased matrix metalloproteinase 9.These biodegradable rhPDGF-BB-loaded membranes were effective in treating diabetic wounds as very advanced accelerators during the initial phases of wound-healing process.     

胆源性慢性胰腺炎动物模型建立初步研究

目的 不完全结扎Wistar大鼠胆总管造成胆道不完全梗阻,观察胰腺的病理学变化,为建立胆源性慢性胰腺炎（BCP）的动物模型做初步可行性探讨.方法 50只Wistar大鼠随机分为三组：空白对照组（10只）、实验对照组（10只）及模型组（30只）.模型组大鼠暴露出胆总管进入十二指肠的根部,游离后用1号可溶性肠线将1枚6号针头连同胆总管一起结扎,然后将针头抽出,关闭腹腔.实验对照组打开腹腔游离出胆总管末端即可.空白对照组不作干预.结果 与对照组比较,模型组大鼠在第3天、第14天以后血胆红素、淀粉酶分别升高,21 d后逐渐出现胰腺腺泡细胞萎缩,纤维组织增生;30 d后腺体萎缩、纤维组织增生更明显;23%模型组大鼠并发胰腺假性囊肿.随着时间的延长,胶原纤维含量逐渐增加.结论 不完全结扎Wistar大鼠的胆总管,30 d即可引起慢性胰腺炎,导致胰腺纤维化.胆总管的不全梗阻在BCP的发病过程中起关键的作用.