Azzarelli B, Muller J, Mirkin L D, Goheen M P
Virchows Arch A Pathol Anat Histopathol. 1985;406(4):425-40. doi: 10.1007/BF00710234.
The possible routes of transvascular migration of leukemic cells in the liver were studied in guinea pigs with an L2C lymphoblastic cell-line inoculation leukemia. Invasion of the hepatic parenchyma theoretically can occur in three ways: Through the intact sinusoidal endothelium, utilizing either preexistent gaps (normal in the liver), or newly created pores, whether interendothelial or intraendothelial. We could not convincingly demonstrate this, but could not wholly exclude this either. After destruction or retraction of the endothelium, either on account of the remarkable sinusoidal engorgement and distension by masses of leukemic cells, or by direct assault on the endothelium by the leukemic cells. We can clearly demonstrate the former, and hold it to be the major cause of hepatic infiltration. Evidence for a direct endotheliolytic effect was not uncovered in our studies. Secondary infiltration from the portal triads. Heavy leukemic infiltration of the triads, whether from the portal or hepatic veins, or from the lymphatics, is indeed and early an consistent feature--but the infiltration of the hepatic lobule shows no peripheral, or any other zonal preference. In both portal and hepatic veins, leukemic cells transverse the endothelium through a cytoplasmic "pore", adjacent to cell junctions, without obvious damage to the endothelium.
在接种L2C淋巴母细胞系白血病的豚鼠中,研究了白血病细胞经血管迁移至肝脏的可能途径。理论上,肝实质的浸润可通过三种方式发生:通过完整的窦状内皮,利用预先存在的间隙(肝脏中正常存在的)或新形成的孔隙,无论是内皮间孔隙还是内皮内孔隙。我们无法令人信服地证明这一点,但也不能完全排除这种可能性。在内皮被破坏或回缩后,这可能是由于大量白血病细胞导致窦状显著充血和扩张,或者是白血病细胞直接攻击内皮。我们能够清楚地证明前者,并认为这是肝脏浸润的主要原因。在我们的研究中未发现直接内皮溶解作用的证据。来自门三联管的继发性浸润。三联管的重度白血病浸润,无论是来自门静脉、肝静脉还是淋巴管,确实是早期且一致的特征——但肝小叶的浸润没有显示出外周或任何其他区域偏好。在门静脉和肝静脉中,白血病细胞通过与细胞连接相邻的细胞质“孔隙”穿过内皮,而对内皮没有明显损伤。