Experimental liver necrosis: hepatic erythrocyte sequestration as a cause of acute anemia.
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.
D000082:Acetaminophen; D000208:Acute Disease; D000740:Anemia / Q000209:etiology* / Q000503:physiopathology; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000503:physiopathology; D004912:Erythrocytes / Q000032:analysis; D005978:Glutathione / Q000032:analysis; D006400:Hematocrit; D008099:Liver / Q000503:physiopathology*; D008297:Male; D009929:Organ Size; D010634:Phenobarbital; D011446:Prospective Studies; D013552:Swine
D000082:Acetaminophen; D005978:Glutathione; D010634:Phenobarbital