Filippeva L A, Tikhonova G N
Arkh Patol. 1975;37(3):37-47.
Genesis of the muscatel-like fibrosis of the liver was studied on section and experimental material. The methods of histological, histochemical and electron microscopy analysis were used. It was established that the rise of pressure in the system of hepatic veins in chronic cardiac decompensation was accompanied by drastic venous congestion, hemorrhages and necrosis of hepacytes in the circumference of the central and collecting veins and along the lines of their junction which resulted in inversion of the hepatic lobes. In the zones of venous congestion pericentral fibrosis developed, which occasionally may be accompanied by priportal fibrosis. At later stages, muscatel-like cirrhosis of the liver was formed. The latter was underlaid by an elevated tropocollagenous activity of cells, this activity apart from fibroplasts, may be fulfilled also by Dupffer's cells. In chronic hepatic congestion a number of compensatory-adaptive changes in the vessels may occur.
在切片和实验材料上研究了葡萄干样肝纤维化的成因。采用了组织学、组织化学和电子显微镜分析方法。结果表明,慢性心功能不全时肝静脉系统压力升高伴有严重的静脉淤血、出血以及中央静脉和集合静脉周围及交界处肝细胞坏死,导致肝叶反转。在静脉淤血区域发生中央周围纤维化,偶尔可伴有门静脉周围纤维化。在后期,形成了葡萄干样肝硬化。后者的基础是细胞原胶原蛋白活性升高,这种活性除了成纤维细胞外,杜氏细胞也可发挥作用。在慢性肝淤血时,血管可能会发生一些代偿性适应性变化。