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目的观察胰淋巴淤滞动物模型胰组织结构变化和胰淀肽沉积情况,探讨淋巴淤滞对胰组织细微和超微结构的影响。方法10月龄大鼠20只,采用腹部结扎大鼠胸导管,建立胰淋巴淤滞动物模型,造模后6个月取材,部分胰组织经石蜡包埋切片,行HE和刚果红染色;部分经冷冻切片,行免疫组织化学染色和光镜观察;部分标本进行透射电镜样品制备和观察。结果HE和刚果红染色切片光镜观察显示,胰腺小叶间隙增宽,呈明显的结缔组织增生、脂肪堆积;胰岛淡染或着朱红色,组织间隙明显增宽。免疫组织化学染色切片光镜观察显示,在胰岛及其周围,呈现胰淀肽强阳性棕褐色着色反应。超薄切片透射电镜观察显示,胰腺小叶间隙增宽,可见血管和扩大的淋巴管;胰岛细胞间隙增宽,细胞间隙内可见大量脂滴样物质和胶原原纤维样结构。结论胸导管结扎可导致胰淋巴引流障碍,引起胰淋巴管扩张,结缔组织间隙增宽,脂肪堆积,胰岛细胞间隙扩大,胰淀肽沉积等,这些结构变化可能影响胰岛的功能。
Objective To observe the changes of pancreatic tissue structure and the deposition of pancreatic amylolide in pancreatic and lymphatic stasis animal models and to explore the effect of lymphatic stasis on the ultrastructure and ultrastructure of pancreatic tissue. Methods Twenty of 10-month-old rats were anesthetized with thoracic duct ligation in the abdomen. Animal models of pancreas-lymphatic stasis were established. Six months after the model was established, some of the pancreatic tissues were paraffin-embedded and stained with HE and Congo red. Frozen sections, immunohistochemical staining and light microscopy; part of the specimens for transmission electron microscopy sample preparation and observation. Results The HE and Congo red sections were observed by light microscopy. The small interphalangeal space of the pancreas was broadened, showing obvious hyperplasia of connective tissue and accumulation of fat. The islets were lightly stained or vermilion, and the interstitial space was obviously widened. Immunohistochemical staining sections of light microscopy showed that in pancreatic islet and its periphery, showing strong positive tan pancreatic peptide coloring reaction. Ultrathin section transmission electron microscopy showed that the pancreatic lobule gap broadened, visible blood vessels and enlarged lymphatic vessels; islet cell gap widened, a large number of lipid droplets visible in the cell gap and collagen fibrillar-like structure. Conclusions Thoracic duct ligation can lead to pancreatic and lymphatic drainage disorders, causing pancreas lymphatic vessels to dilate, widening of connective tissue gap, accumulation of fat, islet cell gap enlargement and deposition of amylin. These structural changes may affect pancreatic islet function.