Prothrombin Activity in Rats with Mammary

The status of hepatic function can be altered by diverse influences. Multiple functional processes are measurably affected by several extrinsic toxic agents (typhoid toxin, chloroform, yellow phosphorus) as well as by a large number of pathological disorders. After exposure to toxins, in obstructive jaundice, in cirrhotic processes, in intrahepatic tumors and the like, either anatomical disruption or functional impairment may first be observed, but generally the two are inseparable. We have recently reported that only after extensive replacement of normal liver tissue by large hepatic tumors induced in rats by p-dimethylaminoazobenzene is the normal capacity of the liver to elaborate prothrombin reduced (4). This condition is not corrected by vitamin K. Furthermore, the anticoagulant, 3,Y-methylenebis (4-hydroxycoumarin), 1 caused a more severe and persistent hypoprothrombinemia in rats with primary hepatic tumors than in normal rats. The purpose of the present report is to indicate that a gross increase in normal hepatic tissue has been observed in rats with spontaneous mammary tumors and that this condition is associated with a greater functional reserve as evidenced by increased plasma prothrombin activity and a reduced hypoprothrombinemic response to a standard dose of 3,3'-methylenebis (4-hydroxycoumarin).