Shibayama Y
J Pathol. 1987 Apr;151(4):315-21. doi: 10.1002/path.1711510412.
The present study was undertaken in rats to examine the significance of sinusoidal circulatory disturbance by microthrombosis in the pathogenesis of hepatic damage and dysfunction due to endotoxin. Administration of endotoxin induced fibrin deposits and infiltration of polymorphonuclear leukocytes in the sinusoids, focal random coagulative hepatocellular necrosis and elevation of serum transaminase activities. When heparin was given simultaneously with endotoxin, the formation of fibrin thrombus in the sinusoids was prevented, and the endotoxin-induced morphological and functional changes in the liver were markedly inhibited. Infusion of thrombin into the portal vein induced a large amount of fibrin thrombi in the sinusoids, focal random necrotic foci resembling the lesions produced by endotoxin and elevation of levels of serum transaminases. These experimental data suggest that disturbance of hepatic microcirculation by sinusoidal thrombosis is the necessary and sufficient condition for the development of endotoxin-induced hepatic injury.
本研究在大鼠中进行，以探讨微血栓形成导致的肝血窦循环障碍在内毒素所致肝损伤和功能障碍发病机制中的意义。给予内毒素可导致肝血窦内纤维蛋白沉积和多形核白细胞浸润、局灶性随机凝固性肝细胞坏死以及血清转氨酶活性升高。当肝素与内毒素同时给予时，可防止肝血窦内纤维蛋白血栓形成，且内毒素诱导的肝脏形态和功能改变受到明显抑制。向门静脉内注入凝血酶可导致肝血窦内大量纤维蛋白血栓形成、出现类似于内毒素所致病变的局灶性随机坏死灶以及血清转氨酶水平升高。这些实验数据表明，肝血窦血栓形成导致的肝微循环障碍是内毒素诱导肝损伤发生的必要充分条件。
