Arai M, Mochida S, Ohno A, Ogata I, Obama H, Maruyama I, Fujiwara K
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Japan.
Thromb Res. 1995 Oct 15;80(2):113-23. doi: 10.1016/0049-3848(95)00157-m.
The regulatory mechanisms of microcirculation might differ in the liver from other organs, because macrophages are resident in the hepatic sinusoids and sinusoidal endothelial cells are unique in shape and function. Thrombomodulin expression in endothelial cells and tissue factor activity in isolated macrophages were studied in the liver and lung of rats. In normal rats, the thrombomodulin expression was minimal in hepatic sinusoids, but prominent in pulmonary capillaries, while the tissue factor activity in the presence of endotoxin was higher in pulmonary macrophages than in Kupffer cells, although the levels in the absence of endotoxin were comparable in both cells. The tissue factor activity in hepatic macrophages was increased after priming of the cells with Corynebacterium parvum or after induction of liver necrosis or cirrhosis with carbon tetrachloride. In the necrotic or cirrhotic liver, increased thrombomodulin expression was seen along capillaries extending in necrotic areas and regenerating nodules, but this increase was minimal in the Corynebacterium parvum-treated rat liver. Blood coagulation equilibrium in microcirculation regulated by endothelial cells and macrophages may differ between the liver and lung. Such equilibrium in the liver may vary depending on pathological status.
肝脏微循环的调节机制可能与其他器官不同,因为巨噬细胞驻留在肝血窦中,且肝血窦内皮细胞在形态和功能上具有独特性。研究了大鼠肝脏和肺中内皮细胞的血栓调节蛋白表达及分离的巨噬细胞中的组织因子活性。在正常大鼠中,肝血窦中的血栓调节蛋白表达极少,而在肺毛细血管中则很显著;尽管在内毒素不存在时两种细胞中的水平相当,但在内毒素存在时,肺巨噬细胞中的组织因子活性高于库普弗细胞。用微小棒状杆菌预处理细胞后,或用四氯化碳诱导肝坏死或肝硬化后,肝巨噬细胞中的组织因子活性增加。在坏死或肝硬化的肝脏中,在坏死区域和再生结节中延伸的毛细血管周围可见血栓调节蛋白表达增加,但在微小棒状杆菌处理的大鼠肝脏中这种增加极少。内皮细胞和巨噬细胞调节的微循环中的血液凝固平衡在肝脏和肺之间可能不同。肝脏中的这种平衡可能因病理状态而异。