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

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
项目状态:
已结题
起止时间:
1990 至 1992

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英文摘要
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
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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)
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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)
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20
    Analysis of Pancreatic Acinar Cell Apoptosis During Acute Pancreatitis
    • 批准号:
      10670495
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $1.73万
    • 财政年份:
      1998
    • 负责人:
      KASHIMA Kei
    • 依托单位:
    Pathophisiological study of acinar cell proliferation and apoptosis
    • 批准号:
      08670609
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $1.6万
    • 财政年份:
      1996
    • 负责人:
      KASHIMA Kei
    • 依托单位:
    Pathophysiological role of CCK in acute experimental pancreatitis
    • 批准号:
      06670573
    • 项目类别:
      Grant-in-Aid for General Scientific Research (C)
    • 资助金额:
      $0.96万
    • 财政年份:
      1994
    • 负责人:
      KASHIMA Kei
    • 依托单位: