Shibayama Y, Hashimoto K, Nakata K
Osaka Medical College, Department of Pathology, Japan.
Exp Pathol. 1991;43(3-4):173-9. doi: 10.1016/s0232-1513(11)80113-1.
The present study was undertaken in rats to clarify whether endotoxin hepatotoxicity can be modified by phagocytic activity of the reticuloendothelial system. Pretreatment with cortisone acetate, diethylstilbestrol, methyl palmitate, triolein or gadolinium chloride markedly improved the mortality rate from endotoxemia and prevented the development of focal random coagulative hepatocellular necrosis and the elevation of serum transaminase activities due to endotoxemia. Cortisone acetate, methyl palmitate and gadolinium chloride are the well-known depressors of reticuloendothelial phagocytic activity: Diethylstilbestrol and triolein are the stimulators. This suggests that phagocytic activity of the reticuloendothelial system does not relate to not only the mortality rate but also the degree of hepatic injury following endotoxemia.
本研究在大鼠中进行,以阐明网状内皮系统的吞噬活性是否能改变内毒素肝毒性。用醋酸可的松、己烯雌酚、棕榈酸甲酯、三油酸甘油酯或氯化钆预处理可显著提高内毒素血症的死亡率,并预防局灶性随机凝固性肝细胞坏死的发生以及内毒素血症引起的血清转氨酶活性升高。醋酸可的松、棕榈酸甲酯和氯化钆是众所周知的网状内皮吞噬活性抑制剂;己烯雌酚和三油酸甘油酯是刺激剂。这表明网状内皮系统的吞噬活性不仅与死亡率无关,而且与内毒素血症后的肝损伤程度也无关。