Studies on pathogenesis and progression of liver cirrhosis -with special reference to the hepatic sinusoidal actomyosin sygtems

透射电镜和免疫组化显示，肝窦内皮细胞、肝星状细胞（Ito细胞）和枯否细胞中存在肌动蛋白和肌球蛋白纤维以及Ca^++>-钙调蛋白肌动球蛋白系统。Fura 2-AM免疫组化和胞浆内游离Ca^++动态分析表明，Ca^++-钙调蛋白肌动球蛋白系统调节窦内皮窗（SEF）的收缩和扩张，扫描电镜和透射电镜观察显示，与对照组相比，SEF的直径和数量明显减少，定量分析表明，肝硬化时枯否细胞对FITC标记内毒素的吞噬活性明显降低。电镜观察证实，与对照组相比，肠系膜静脉导管注入的微粒在肝硬化肝Disse间隙内减少，提示肝窦血流量减少的加重是由于SEF直径和数量减少以及枯否细胞吞噬活性降低所致。两者均与急性肝损伤时血清内毒素水平升高有关。

By transmission electron microscopy and immunohistochemistry, actin and myosin filaments and Ca^<++>-calmodulin actomyosin system are evident in the hepatic sinusoidal endothelial cells, hepatic stellate cells (Ito cells) and Kupffer cells. Immunohistochemistry and the dynamic analysis of intracytoplasmic free Ca^<++> ion using Fura2-AM showed that the Ca^<++> -calmodulin actomyosin system regulates the contraction and dilatation of the sinusoial endothelial fenestrae (SEF), contaction of Ito cells and phagocytotic activities of Kupffer cells.Scanning and transmission electron microscopy revealed that the diameter and numbers of the SEF were significantly decreased concomitant with the fibrosis within the space of Disse in cirrhotic liver.By quantitative analysis, the phagocytotic activity of Kupffer cells against the FITC-labelled endotoxin have been shown to be significantly decreased in cirrhotic liver. Furthermore, electron microscopic observations have proved that the microparticles injected via a mesenteric vein catheter are decreased in space of Disse in cirrhotic liver as compared with control liver.These finding may indicate that the enhancement of a decrease of hepatic sinusoidal blood flow results from a decrease of SEF in diameter and number and a decrease of phagocytotic activity of Kupffer cells, both of which have some relationship with an increase of serum endotoxin levels in cirrhotic liver.