Asaka S, Shibayama Y, Nakata K
Department of Pathology, Osaka Medical College, Japan.
Liver. 1996 Jun;16(3):183-7. doi: 10.1111/j.1600-0676.1996.tb00725.x.
The present study was undertaken in rats to clarify the role of sinusoidal circulatory disturbances due to fibrin thrombi in the development of focal and random hepatocellular necrosis in endotoxemia. Sinusoidal circulation was examined microscopically in vivo in rats injected with endotoxin or heparin, or both. The sinusoids in places were occluded by adherent fibrin and neutrophils soon after endotoxin injection, and subsequently the sinusoidal blood flow stagnated, reversed, or detoured. Most of these sinusoidal circulatory disturbances recovered in a few hours. However, when the sinusoidal occlusion developed simultaneously in clusters of adjacent sinusoids, the sinusoidal circulatory disturbance persisted and induced ischemic foci and then hepatocellular coagulative necrosis. Pretreatment with heparin definitely prevented the adherence of fibrin and neutrophils to the sinusoidal walls, and focal hepatocellular necrosis did not appear. These results suggest that focal and random hepatocellular necrosis in endotoxemia is caused by circulatory disturbances due to fibrin thrombi in clusters of adjacent sinusoids.
本研究在大鼠身上进行，以阐明内毒素血症中纤维蛋白血栓引起的肝血窦循环障碍在局灶性和随机性肝细胞坏死发展过程中的作用。通过显微镜观察注射内毒素或肝素或两者的大鼠体内的肝血窦循环。内毒素注射后不久，局部肝血窦被黏附的纤维蛋白和中性粒细胞阻塞，随后肝血窦血流停滞、逆流或迂回。这些肝血窦循环障碍大多在数小时内恢复。然而，当相邻肝血窦群同时出现肝血窦阻塞时，肝血窦循环障碍持续存在并诱导缺血灶，进而导致肝细胞凝固性坏死。肝素预处理确实可防止纤维蛋白和中性粒细胞黏附于肝血窦壁，且未出现局灶性肝细胞坏死。这些结果表明，内毒素血症中的局灶性和随机性肝细胞坏死是由相邻肝血窦群中的纤维蛋白血栓引起的循环障碍所致。
