一种研究急性胰腺炎加重病理机理的动物模型

介绍一种急性水肿性胰腺炎（ＡＥＰ）向坏死性胰腺炎（ＡＮＰ）转变的大鼠模型。１０７只ＳＤ大鼠随机分为假手术组、ＡＥＰ组和ＡＮＰ组。ＡＥＰ通过胰管结扎、外分泌刺激诱发。在ＡＥＰ模型基础上静注大剂量Ｄｅｘｔｒａｎ１１０诱发ＡＮＰ。结果显示：血清淀粉酶水平在ＡＥＰ、ＡＮＰ组明显增高，胰腺泡细胞胞浆游离钙离子浓度在ＡＮＰ诱发后持续增高；胰腺出血、实质坏死、钙沉积在ＡＮＰ组常见。超微结构显示ＡＮＰ组胰毛细血管内皮剥脱、坏死。由此表明，胰腺缺血可能通过腺泡细胞钙超负荷的作用促发ＡＥＰ向ＡＮＰ转变。该大鼠模型因临床联系较好、病变渐进，不失为一种从细胞和分子水平研究急性胰腺炎加重病理机理的动物模型

A ANIMAL MODEL FOR STUDY OF THE AGGRAVATING MECHANISM OF ACUTE PANCREATITIS

To introduce a rat model of the conversion of acute edematous pancreatitis (AEP) to necrotizing pancreatitis (ANP). One hundred and seven Sprague Dawley rats were randomized in three experimental groups as follows: sham operation control group and AEP group and ANP group. AEP was induced by pancreatic duct ligation and exocrine stimulation, ANP was induced same as AEP,but with a large dose of dextran 110 (500mg/kg) intravenously. The serum concentration of amylase increased significantly in AEP group and ANP group. Cytosolic free Ca 2 concentration in isolated pancreatic acinar cells increased consistently after induction of ANP. Homorrhage, parenchymal necrosis and calcium deposits in acinar cells were observed in pancreas in ANP group. Ultrastructural examination showed desquamation and necrosis of the endothelium of the pancreatic capillary in ANP group. These results suggest that ischemia may induce the conversion of AEP to ANP via acinar cell Ca 2 overloading. The rat model would seem to be a suitable animal model for studying aggravating mechanism of acute pancreatitis.