Studies on the Endotoxin Shock

细菌脂多糖（LPS）刺激后，大量的炎症细胞如白细胞和巨噬细胞聚集并粘附于血管内皮表面。在LPS处理的样品中，还存在显著的内皮细胞损伤，包括胞浆内水肿、自噬空泡数量增加和细胞间连接扩张。脂多糖处理组肝实质细胞变性，如肝细胞坏死、肾近端小管细胞坏死和心肌细胞水肿。在LPS处理的样品中检测了白三烯（LT）和肿瘤坏死因子（TNF）的免疫细胞化学产物的存在。在粘附于内皮细胞表面的炎性细胞溶酶体中观察到的LT免疫反应可能表明内皮细胞损伤的发生。TNF在内皮细胞表面的阳性免疫反应表明TNF可增强白细胞与内皮细胞的粘附。除了这些反应部位外，肝、肾近端小管细胞坏死和心肌水肿等实质细胞变性的溶酶体也呈TNF或LT免疫反应。这些实质细胞变性主要是由内源性TNF或LT引起的，而不是由缺血引起的。

Abundant inflammatory cells such as leukocytes and macrophages accumulated and adhered to the endothelial surface of the vascular vessels after administration of bacterial lipopolysaccharide(LPS). There is also marked endothelial cell damage including intracytoplasmic edema, increased numbers of autophagic vacuoles and dilatation of the intercellular junction in LPS-treated samples. The degeneration of parenchymal cells such as hepatic necrosis, renal proximal tubular cell necrosis and edematous muscle cells of the myocardium also observed in LPS-treated sample. The presence of immunocytochemical products of leukotriene(LT) and tumor necrosis factor(TNF) was examined using in LPS-treated samples. Immunoreactions of LT seen in the lysosomes of inflammatory cells attached to the endothelial cell surface may indicate the onset of endothelial cell damage. Positive immunoreactions of TNF on the endothelial cell surface indicate that TNF may enhance the adhesion of leukocytes to endothelium. In addition to these reactios sites, lysosomes of the degeneration of parenchymal cells such as hepatic necrosis, renal proximal tubular cell necrosis and edematous muscle cells of the myocardium were immunoreactive for TNF or LT.These degeneration of parenchymal cells is primarily caused by endogenous TNF or LT rather than by ischemia.