Rappaport A M, MacPhee P J, Fisher M M, Phillips M J
Virchows Arch A Pathol Anat Histopathol. 1983;402(2):107-37. doi: 10.1007/BF00695054.
Cirrhosis is defined as the scarring of the liver acini in zone 3, zone 1 or in both; the resulting nodules are scarred and modified remnants of acini of various orders. The division of the nodules into "micronodules" and "macronodules" is difficult to justify as their two dimensional appearance changes at different planes of section. Early scar formation precedes changes in the microcirculatory dynamics. Sprouting of vascular branches, especially of arterioles, takes the leading role in the development of mature scars, i.e. of fibro-vascular membranes. The fibrous repair is at the same time the road builder for collateral flow. The pathophysiology of the collateral circulation is the basic determinant in the formation of the cirrhotic patterns. The three microcirculatory phases in the cirrhotic process are due to a changeover of the intrahepatic circulatory path from the normal trichotomy of the preterminal vascular branches to convoluted collateral channels. The three phases of the cirrhotic process are: The Triadal Nodule. It receives blood from the TPV and THA and from the perinodular plexus. The nodular parenchyma may already be segregated from the ThV, a situation that leads to portal hypertension. The Para-triadal Nodule. It is a conglomerate of nodules that often are not completely separated from each other; they are derived from neighbouring acini of various orders which receive blood from large triads contained in the perinodular scar. The blood arrives into the sinusoids primarily via the perinodular plexus. Some sinusoids may receive additional blood through sclerosing remnants of terminal afferent branches and through irregular vascular twigs which, along with septa, enter the nodules at various sites. The A-triadal Nodule. It is completely separated from neighbouring nodules by thick scars, its parenchyma totally segregated from afferent and efferent vascular branches. The nodules receive blood only from a dense perinodular plexus of wide capillaries.
肝硬化的定义为肝腺泡3区、1区或两区同时出现瘢痕形成；由此产生的结节是不同级别的腺泡瘢痕化和改变后的残余部分。由于结节在不同切片平面上的二维外观会发生变化，因此将其分为“微结节”和“大结节”很难说得通。早期瘢痕形成先于微循环动力学的改变。血管分支，尤其是小动脉的芽生，在成熟瘢痕即纤维血管膜的形成中起主导作用。纤维修复同时也是侧支循环的通路构建者。侧支循环的病理生理学是肝硬化模式形成的基本决定因素。肝硬化过程中的三个微循环阶段是由于肝内循环路径从终末前血管分支的正常三分法转变为迂曲的侧支通道所致。肝硬化过程的三个阶段如下：三联结节。它从门静脉主干、肝动脉和结节周围丛状血管接收血液。结节实质可能已经与肝静脉分离，这种情况会导致门静脉高压。旁三联结节。它是结节的聚集体，通常彼此并未完全分离；它们源自不同级别的相邻腺泡，这些腺泡从结节周围瘢痕中包含的大三联体接收血液。血液主要通过结节周围丛状血管进入血窦。一些血窦可能通过终末传入分支的硬化残余以及不规则的血管小分支接收额外的血液，这些血管小分支与间隔一起在不同部位进入结节。A三联结节。它被厚厚的瘢痕与相邻结节完全隔开，其实质与传入和传出血管分支完全分离。这些结节仅从密集的宽毛细血管结节周围丛状血管接收血液。
