Meister R, Berger I, Schwille P O, Gebhardt C
Division of Experimental Surgery, University of Erlangen-Nürnberg, FRG.
Eur J Surg. 1991 May;157(5):333-40.
The response of the pancreatic islet A- and B-cells after long-standing (eight years) pancreatic duct occlusion by prolamine, and subsequently developed acinar atrophy, was studied in five beagles, and the results compared with those in six sham-operated dogs. Intravenous arginine infusion (A-cell stimulation) and a combined oral glucose and intravenous tolbutamide and glucagon infusion (B-cell stimulation) were carried out in each dog. Complete abolition of acinar function after duct occlusion was documented by the negative paraaminobenzoic acid test. In contrast, in plasma, baseline values of glucose, alpha-amino-nitrogen, insulin, glucagon, glucagon-like immunoreactivity, somatostatin-like immunoreactivity, and pancreatic polypeptide did not differ between the experimental groups. During B-cell stimulation dogs with occluded ducts had significantly reduced insulin, reduced glucagon, and reduced second phase pancreatic polypeptide compared with controls. Integrated insulin and pancreatic polypeptide were also reduced in dogs with occluded ducts. In both groups plasma and integrated values of glucose and somatostatin-like immunoreactivity did not differ. During the A-cell stimulation period dogs with occluded ducts had significantly raised alpha-amino-nitrogen but unchanged glucose and reduced insulin concentrations; in both groups the arginine-induced rise in glucagon was similar, although it was delayed in the experimental group. In the latter, integrated alpha-amino-nitrogen was raised, but integrated glucose and hormones were unchanged. We conclude that a previously intact dog pancreas that has been atrophied by duct occlusion, may be able to maintain euglycaemia for several years. There may be a complex interplay of changes induced by duct occlusion at the level of the pancreatic islets and elsewhere, which compensate for moderate insulinopenia.
在五只比格犬中研究了用醇溶蛋白进行长期（八年）胰管闭塞并随后出现腺泡萎缩后胰岛A细胞和B细胞的反应，并将结果与六只假手术犬的结果进行比较。对每只犬进行静脉注射精氨酸（刺激A细胞）以及口服葡萄糖、静脉注射甲苯磺丁脲和胰高血糖素联合注射（刺激B细胞）。通过对氨基苯甲酸试验阴性证明了导管闭塞后腺泡功能完全丧失。相比之下，在血浆中，实验组之间葡萄糖、α-氨基氮、胰岛素、胰高血糖素、胰高血糖素样免疫反应性、生长抑素样免疫反应性和胰多肽的基线值没有差异。在B细胞刺激期间，与对照组相比，导管闭塞的犬胰岛素显著降低，胰高血糖素降低，第二阶段胰多肽降低。导管闭塞的犬的整合胰岛素和胰多肽也降低。两组中葡萄糖和生长抑素样免疫反应性的血浆和整合值没有差异。在A细胞刺激期间，导管闭塞的犬α-氨基氮显著升高，但葡萄糖不变，胰岛素浓度降低；在两组中，精氨酸诱导的胰高血糖素升高相似，尽管在实验组中延迟。在后者中，整合的α-氨基氮升高，但整合的葡萄糖和激素不变。我们得出结论，先前完整的犬胰腺因导管闭塞而萎缩后，可能能够维持数年的血糖正常。在胰岛和其他部位，导管闭塞引起的变化可能存在复杂的相互作用，可补偿中度胰岛素缺乏。
