Mundlos S, Adler G, Schaar M, Koop I, Arnold R
Pancreas. 1986;1(1):29-36. doi: 10.1097/00006676-198601000-00007.
Pancreatic insufficiency was induced in rats by a single injection of 50 microliter oleic acid into the pancreatic duct over a period of 3 min. Exocrine tissue was destroyed within 3-6 days, and after 6 weeks the remaining pancreas equaled 2.7% of the original organ. The rats showed retardation of body weight in spite of normal food intake. After 7 weeks the fecal weight increased by 23%, and the fecal chymotrypsin activity decreased by 90% compared to controls. At this time plasma cholecystokinin (CCK) concentrations were significantly elevated. The amylase content in the remaining pancreas was reduced by 99%, and trypsin content was reduced by 93%. Unstimulated protein discharge from the remnant pancreas in vitro was threefold higher compared to secretion from control tissue. Thus a simple, reproducible model for inducing persistent pancreatic insufficiency was developed. To compensate for the loss of exocrine tissue, the remaining acinar cells adapt by a CCK-mediated increase in protein secretion.
通过在3分钟内将50微升油酸单次注射到大鼠胰管中诱导胰腺功能不全。外分泌组织在3 - 6天内被破坏,6周后剩余的胰腺仅为原始器官的2.7%。尽管食物摄入量正常,但大鼠体重增长迟缓。7周后,粪便重量增加了23%,粪便糜蛋白酶活性与对照组相比降低了90%。此时血浆胆囊收缩素(CCK)浓度显著升高。剩余胰腺中的淀粉酶含量降低了99%,胰蛋白酶含量降低了93%。与对照组织的分泌相比,体外剩余胰腺未受刺激时的蛋白质分泌量高出三倍。因此,开发出了一种简单、可重复的诱导持续性胰腺功能不全的模型。为了补偿外分泌组织的损失,剩余的腺泡细胞通过CCK介导的蛋白质分泌增加来进行适应。