Pathogenesis of a rat model of chronic pancreatic insufficiency induced by injection of zein-oleic acid-linoleic acid solution into the pancreatic duct

胰管注射玉米醇溶蛋白-油酸-亚油酸溶液致慢性胰功能不全大鼠模型的发病机制

• 批准号: 02670313
• 负责人: KASHIMA Kei
• 金额: $ 1.28万
• 依托单位: Kyoto Prefectural University of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1990
• 资助国家: 日本
• 起止时间: 1990 至 1992
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-02670313/
• 关键词: A rat model of chronic pancreatic insufficiency; zein-oleic acid-linoleic acid solution; into the pancreatic duct; biochemical study; histological study; 膵外分泌機能; Zein-oleic acid-1inoleic acid溶液; ラット; 慢性膵外分泌不全モデル; Zein‐oleic acid‐linoleic acid溶液 /

An experimental model of chronic pancreatitis was induced by a retrograde injection of the viscous solution consisting of zein-oleic acid-linoleic acid (0.05ml/100g BW) into the rat pancreatic duct. Serial microscopic studies revealed that the injected solution remained at least over 24 hr mainly in interlover ducts and partially in intralobar ducts, whereas the solution in the common bile-pancreatic duct was immediately washed out into the duodenum. The early ultra-structural changes of acinar cells were observed as decrease in zymogen granules and dilatation of the endoplasmic reticulum. Widening of acinar lumen and cellular vacuolization occurred within 24 hr at the parenchyma neighboring the small ducts filled with the zein-solution. Further decrease in cell height and dilatation of acinar lumen were accumulated and interstitial edema accompained with cellular infiltration was pronounced at 1 week. Degeneration of acini showing as tubular complexes appearance progressed afterward a … More nd led to marked atrophy with irregular fibrosis and fat replacement over a period of 6 months. In addition, irregular dilatation of major pancreatic duct and its branches with periductal fibrosis was observed at 6 months.Serum amylase level which was maximally increased 6 h after the injection was normalized on the second day and this level persisted for 6 months. As time passed, the treated rats gained weight gradually but pancreatic weight was reduced (-33% after 1 week, -69% after 6 weeks, -88% after 6 months). Pancreatic contents of protein, amylase, DNA and RNA were distinguishedly decreased as well as pancreatic weight, while hydroxyproline content was apparently increased. BT-PABA test was indicated as 54% at 6 weeks and 22% at 6 months. Although three quarters of pancreatic IRI content was lost after 6 months, overt diabetes did not occurred.Based on these results, it was considered that obstructive changes in the small ducts might play an important role in genesis and development of chronic pancreatitis. Less

将玉米醇溶蛋白-油酸-亚油酸组成的粘稠溶液（0.05ml/100 gBW）逆行注入大鼠胰管，造成慢性胰腺炎模型。系列显微镜研究显示，注射溶液主要保留在肝间管和部分叶内管中至少超过24小时，而胆胰总管中的溶液立即被冲洗到十二指肠中。早期腺泡细胞超微结构改变为酶原颗粒减少，内质网扩张。腺泡腔变宽和细胞空泡化发生在24小时内在薄壁组织附近的小导管充满玉米醇溶蛋白溶液。1周时细胞高度进一步降低，腺泡腔扩张，间质水肿伴细胞浸润。腺泡变性，表现为管状复合体的出现， ...更多信息 ND导致6个月内明显萎缩伴不规则纤维化和脂肪替代。6个月时胰管及其分支不规则扩张，胰管周围纤维化，血清淀粉酶水平在注射后6 h最高，第2天恢复正常，并持续6个月。随着时间的推移，治疗的大鼠体重逐渐增加，但胰腺重量减少（1周后-33%，6周后-69%，6个月后-88%）。胰腺蛋白质、淀粉酶、DNA和RNA含量明显降低，羟脯氨酸含量明显升高，胰腺重量明显减轻。BT-PABA试验显示6周时为54%，6个月时为22%。虽然6个月后胰腺IRI含量减少了四分之三，但未出现明显的糖尿病，因此认为小导管的阻塞性改变在慢性胰腺炎的发生和发展中起重要作用。少

项目成果

頼住 一: "消化器疾患の防御機構" 現代医療社, 110 (1991)

Hajime Yorizumi：“消化系统疾病的防御机制”Gendai Iryosha，110（1991）

片岡 慶正: "膵炎の発症と進展" 東洋書店, 96 (1992)

片冈义正：“胰腺炎的发病和进展”东洋书店，96（1992）

"Characterization of Muscarinic Reseptor Subtipes on Rat Pancreatic Acini:Pharmacological Identification by Secretory Responses and Binding Studies." DIGESTION. 52. 194-203 (1992)

“大鼠胰腺腺泡毒蕈碱受体亚型的表征：通过分泌反应和结合研究进行药理学鉴定。”

Kei, KASHIMA: "Nutritional Management of Patients with Chronic Pancreatitis." J. Bil. Panc.Vol.13. 369-373 (1992)

Kei, KASHIMA：“慢性胰腺炎患者的营养管理。”

Hajime, YORIZUMI: GENDAIIRYOSHA. Defense Mechanism of Digestive Disease, 110 (1991)

赖泉肇：现代入社。