Miller D J, Pichanick G G, Fiskerstrand C, Saunders S J
Am J Dig Dis. 1977 Dec;22(12):1055-9. doi: 10.1007/BF01072856.
A prospective study was undertaken to determine the cause of the acute anemia previously observed in pigs manifesting acute liver necrosis after administration of acetaminophen in dosages in excess of the LD100. A highly significant correlation was found between the degree of anemia and increase in liver weight (P less than 0.001) and a similarly significant correlation was noted between the increase in liver weight and 51Cr activity in the liver after administration of autologous erythrocytes labeled with 51Cr. Marked hepatic erythrocyte sequestration was confirmed histologically, whereas there was minimal erythrocyte accumulation in extrahepatic tissue. Erythrocyte glutathione content was not altered by acetaminophen administration. It was concluded that hepatic sequestration of erythrocytes occurred to a sufficient extent to account for the precipitous fall in hematocrit observed.
进行了一项前瞻性研究，以确定之前在用超过LD100剂量的对乙酰氨基酚给药后出现急性肝坏死的猪中观察到的急性贫血的原因。发现贫血程度与肝脏重量增加之间存在高度显著相关性（P小于0.001），并且在用51Cr标记的自体红细胞给药后，肝脏重量增加与肝脏中51Cr活性之间也观察到类似的显著相关性。组织学证实存在明显的肝脏红细胞滞留，而肝外组织中的红细胞积聚极少。对乙酰氨基酚给药未改变红细胞谷胱甘肽含量。得出的结论是，红细胞在肝脏中的滞留程度足以解释观察到的血细胞比容急剧下降。
