Lunam C A, Hall P M, Cousins M J
Department of Anatomy and Histology, School of Medicine, Flinders University of South Australia, Bedford Park.
Br J Exp Pathol. 1989 Oct;70(5):533-41.
The pathology of halothane hepatotoxicity is described in detail in a guinea-pig model. Twenty-two of 40 guinea-pigs developed liver damage after exposure to 1% halothane in 21% O2 for 4 h. The other 18 animals showed no evidence of hepatic injury. Two distinct patterns of damage were identified: mild damage, in which livers had focal areas of necrosis, and severe damage, where necrosis was confluent around the terminal hepatic venules, often extending to the portal tracts. Serum alanine aminotransferase activity was significantly elevated in guinea-pigs with severe liver damage. Hepatocytes in the damaged areas showed degenerative changes ranging from vacuolization to ballooning degeneration and necrosis. Inflammatory cells, predominantly lymphocytes, were often present in the areas of necrosis. The pathology of mild and severe liver injury in the guinea-pig closely resembles the spectrum of injury observed in non-fatal halothane hepatitis in man.
在豚鼠模型中对氟烷肝毒性的病理学进行了详细描述。40只豚鼠中有22只在暴露于含21%氧气的1%氟烷中4小时后出现肝损伤。另外18只动物未显示肝损伤迹象。确定了两种不同的损伤模式：轻度损伤，肝脏有局灶性坏死区域；重度损伤，终末肝小静脉周围坏死融合，常延伸至门管区。重度肝损伤的豚鼠血清丙氨酸转氨酶活性显著升高。受损区域的肝细胞呈现从空泡化到气球样变性和坏死的退行性变化。坏死区域常存在以淋巴细胞为主的炎症细胞。豚鼠轻度和重度肝损伤的病理学与人类非致命性氟烷肝炎中观察到的损伤谱非常相似。
