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牛肝脏的毛细血管前扩张和毛细血管扩张:一项形态学、免疫组织化学和超微结构研究。

Pretelangiectasis and telangiectasis of the bovine liver: a morphological, immunohistochemical and ultrastructural study.

作者信息

Marcato P S, Bettini G, Della Salda L, Galeotti M

机构信息

Department of Veterinary Public Health and Animal Pathology, University of Bologna, Italy.

出版信息

J Comp Pathol. 1998 Aug;119(2):95-110. doi: 10.1016/s0021-9975(98)80055-8.

Abstract

Forty-five livers from conventionally slaughtered Holstein-Friesian steers with telangiectasis were studied by histochemical methods, immunolabelling for fibronectin, laminin and type IV collagen, and transmission electron microscopy. None of the previously described changes in telangiectasis (necrosis, hepatitis, thromboembolism, dilatation of the space of Disse by glycogen extruded from hepatocytes and reduced density of the perisinusoidal reticulin framework) were evident. Pretelangiectasis (sinusoidal dilatation) and telangiectasis (blood-filled cavities) were characterized by sinusoidal barrier alterations, leading to sinusoidal capillarization; and there was progressive formation of a true basement membrane and perisinusoidal fibrosis. Comparison of bovine liver telangiectasis and human peliosis hepatis suggests that they have a similar pathogenesis. It is suggested that a primary alteration of the sinusoidal barrier is responsible for an increased deposition of basement membrane components (fibronectin, laminin, type IV collagen) in the perisinusoidal region, and fibrosis. These are likely to render the exchange of oxygen and substrates between blood and hepatocytes more difficult and to produce haemodynamic imbalances, leading to hepatocyte atrophy and eventually to sinusoidal disruption.

摘要

采用组织化学方法、纤连蛋白、层粘连蛋白和IV型胶原免疫标记以及透射电子显微镜技术,对45例来自传统屠宰的患有毛细血管扩张的荷斯坦 - 弗里生公牛肝脏进行了研究。先前描述的毛细血管扩张的变化(坏死、肝炎、血栓栓塞、肝细胞挤出的糖原导致狄氏间隙扩张以及肝血窦周网状纤维框架密度降低)均不明显。毛细血管扩张前期(肝血窦扩张)和毛细血管扩张期(充血腔)的特征是肝血窦屏障改变,导致肝血窦毛细血管化;并且有真正基底膜和肝血窦周纤维化的进行性形成。牛肝脏毛细血管扩张与人类肝紫癜的比较表明它们具有相似的发病机制。有人提出,肝血窦屏障的原发性改变是基底膜成分(纤连蛋白、层粘连蛋白、IV型胶原)在肝血窦周区域沉积增加和纤维化的原因。这些可能会使血液与肝细胞之间的氧气和底物交换更加困难,并产生血流动力学失衡,导致肝细胞萎缩并最终导致肝血窦破裂。

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