Seelig R, Seelig H P, Rohnaeher R
Z Gastroenterol. 1976 Oct;14(6):654-67.
Acute necrotizing pancreatitis was introduced in rats by intrapancreatic complement activation. As an immunopathogenetic model for complement activation an intrapancreatic Arthus reaction was produced by intraductal injection of rabbit IgG into sensitized animals. Antibody independent complement activation was accomplished by intraductal injection of particulated inulin and cobra venom factor resp. As shwon by histological and immunohistological examination the development of acinar cell necroses and the consecutive inflammatory reaction followed an identical course in all three models. The generation of cytolytically active complement is suggested to be the common link in the formal pathogenesis of the initial membrane demage of the acinar cells which enables its autodigestion by pancreatic enzymes. The region of the initial complement activation within the pancreas but not the mode of its activation (by immunological or non-immunological processes) determine the topography of acinar cell necroses and connective tissue proliferation.
通过胰腺内补体激活在大鼠中诱发急性坏死性胰腺炎。作为补体激活的免疫病理发生模型，通过向致敏动物的导管内注射兔IgG产生胰腺内阿瑟斯反应。分别通过导管内注射颗粒状菊粉和眼镜蛇毒因子实现抗体非依赖性补体激活。组织学和免疫组织学检查显示，在所有三种模型中，腺泡细胞坏死的发展以及随后的炎症反应过程相同。细胞溶解性活性补体的产生被认为是腺泡细胞初始膜损伤的正式发病机制中的共同环节，这种损伤使其能够被胰酶自身消化。胰腺内初始补体激活的区域而非其激活方式（通过免疫或非免疫过程）决定了腺泡细胞坏死和结缔组织增殖的形态。
