Hepatic dearterialization in 3'-methyl-4-dimethylaminoazo-benzene-induced hepatocellular carcinoma with special reference to circulatory dynamics and mitochondrial functions.

This time trend of hemodynamics and mitochondrial functions were studied to determine whether the ligation of the hepatic artery would result in an antitumor effect on 3'-methyl-4-dimethylaminoazobenzene-induced hepatic carcinoma in rats. The studies revealed that the hepatic tumors were nourished predominantly by the artery and less by the portal vein; the size of the vascular beds in the hepatic tumors decreased as compared with those in the non-tumor area; and as the tumors grew larger, the artery became less predominant and the size of vascular beds decreased further. The mitochondria in the tumor were characterized by impaired growth, impaired oxidative phosphorylation, and by the low activity and nucleotide specificity of membrane bound ATPase. Hepatic dearterialization enhanced ischemia in the tumors and was accompanied by intensified impairment of the aerobic energy production, resulting in necrosis of the tumor. The effects of the dearterialization tended to decrease after the 5th day following the operation. In view of the gross findings upon relaparotomy and the recovery of hemodynamics and mitochondrial functions, this tendency appeared to be chiefly attributed to the increasing collateral circulation.