Kishimoto S, Shimizu S, Kambara A, Okamoto K, Koh H, Yamamoto M, Tamaru T, Kajiyama G, Miyoshi A, Yanaihara N
Peptides. 1984 Mar-Apr;5(2):451-8. doi: 10.1016/0196-9781(84)90253-5.
Morphological, ultrastructural, and immunocytochemical studies of nerves containing vasoactive intestinal peptide (VIP) are described in diabetic pancreas of rats after streptozotocin treatment. The observations covered 48 hours and 6 months following streptozotocin treatment. At the ultrastructural level, degenerative changes were already observed in axons of nerve ganglia in the pancreas 48 hours (early stage) after streptozotocin treatment. These changes were hardly detected at the light microscopic level and VIP-like immunoreactivities were seen in nerves and fibers in such pancreas. The nerve ganglia were almost absent in the diabetic pancreas 6 months after streptozotocin treatment (late stage). Associated with the absence of nerve ganglia, nerves and fibers containing VIP-like immunoreactivities were also absent at this late stage. The findings indicated that the changes in the diabetic pancreas were neuropathic caused by metabolic disturbance after long standing diabetes and resulting absence of VIP-like immunoreactive nerves occurred. It was suggested from the present study that the changes in nerve ganglia began as damage at the ultrastructural level due to acute toxicity of the chemical at an early stage and then developed destruction and absence at a late stage.
本文描述了链脲佐菌素处理后大鼠糖尿病胰腺中含血管活性肠肽(VIP)神经的形态学、超微结构和免疫细胞化学研究。观察时间涵盖链脲佐菌素处理后的48小时和6个月。在超微结构水平上,链脲佐菌素处理后48小时(早期)胰腺神经节的轴突就已出现退行性变化。这些变化在光学显微镜下很难检测到,并且在此类胰腺的神经和纤维中可见VIP样免疫反应性。链脲佐菌素处理6个月后(晚期)糖尿病胰腺中几乎没有神经节。与此神经节缺失相关,此晚期也不存在含VIP样免疫反应性的神经和纤维。研究结果表明,糖尿病胰腺的变化是由长期糖尿病后的代谢紊乱引起的神经病变,导致VIP样免疫反应性神经缺失。本研究表明,神经节的变化在早期因化学物质的急性毒性而始于超微结构水平的损伤,然后在晚期发展为破坏和缺失。