The effects of phenobarbital (PB) and bucolome (BC) on dye metabolism (bilirubin, BSP, ICG) were studied in Sprague-Dawley (SD) rats, Gunn rats and mongrel dogs.
Daily administration of both PB (i.m.) and BC (i.p.) for 5 days caused a decrease in the serum bilirubin levels in Gunn rats and an increase in plasma clearance rate of ICG and BSP in both rats. PB caused a significant increase in hepatic glucuronyltransferase activity and Y protein (p<0.01), while BC caused no changes in these values. Intravenous injection of BC was followed by a remarkable increase in portal flow of dogs and bile flow of rats, but PB resulted in no such changes. Binding capacity of serum protein to ICG was more markedly increased by BC than by PB.
It seems that the effects of BC on dye metabolism are due to the increase in hepatic blood flow and bile flow and to the changes in serum protein.

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Two ml of the hemolysate prepared from rat erythrocytes was administered intraperitonealy to rats once a week for six months. Then the liver was examined morphologically and functionaly.
In the morphological studies, the liver cell degeneration, decrease content of PAS positive substance of hepatocyte and slight fibrosis were observed. The erectron lucent vacuoles with single membrane were seen along the sinusoidal surface of hepatocyte and collagen fiber were ploriferated in the space of Disse which was not uniform in width. The cytoplasmic process of endotherial lining of sinusoid became so thick that no fenestration was observed. It was estimated that these sinusoidal changes was identical with so called "capillarization" of sinusoid.
In the functional studies, serum GOT, GPT and Al-P were in normal range, but 131I-BSP retention rate in the rats administered hemolysate were more increased than that in the control.
From these results, it might be concluded that some substaces in the hemolysate cause the damages of the liver tissue, especially sinusoidal walls.

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Several investigators^1-7) have reported the sporadic cases in which plasma clearance of Indocyanine Green (ICG) was remarkably delayed whereas plasma decay of sulfobromophthalein sodium (BSP) was normal. Namihisa et al.⁸⁾, reporting this condition in a male and his father, discussed that this condition might be constitutional.
We identified 5 such individuals without overt liver disease in a highly consanguineous Japanese kindred and some studies were conducted to elucidate the pathophysiological basis of this phenomenon and to determine the mode of transmission of this trait.

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A significant rise in serum γ-glutamyl transpeptidase (γ-GTP) was observed in 75% of epileptic patients without clinical evidence of liver disease. γ-GTP elevation was closely related to multiple anticonvulsant drugs therapy. The possibility that serum γ-GTP elevation could result from release of anticonvulsant drugs-induced hepatic γ-GTP but not from concomitant liver damage due to these drugs is discussed.

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A combined administration of tetrakis (nicotinoyloxymethyl) cyclohexanol (Nicomol) and ethyl α-(p-chlorophenoxy)-isobutyrate (CPIB) to a case of familial type II hyperlipoproteinemia gave results suggestive of an additive lipid-lowering effect of these two compounds.
In an attempt to prove this results, effects of the two compounds on metabolite and enzyme levels were studied with rats.
Liver weight and contents of liver protein and total phospholipid were increased by a factor of about 1.5 and liver glycogen content was significantly decreased in CPIB treated rats. In Nicomol-fed rats, these changes were not observed.
Serum triglyceride concentration decreased with each compound, although the additive lipid-lowering effect of the two compounds was not observed with rats.
Activities of microsomal drug-metabolizing enzymes tended to increase slightly with Nicomol and significantly increased with CPIB.
Glucokinase, hexokinase and glucose 6-phosphate dehydrogenase activities were not significantly changed in livers of Nicomol-fed rats. In rats fed CPIB or both compounds, these enzyme activities changed significantly without showing liver cell injury.

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This is a report of a case of a 69-year-old male with primary hepatic cancer and sarcoma. Alcoholism was not mentioned in his history. During his hospitalizing period, he complained anorexia and easy fatigability. Ascites and edema of lower extremities were prominent in the terminal stage. Laboratory findings showed an elevated s-GOT and s-GPT level and hypergammaglobulinemia. At necropsy, 2 tumors were found in the liver besides distinct portal cirrhosis. The larger tumor found in the right lobe was a typical spindle cell sarcoma and the smaller tumor found in the left lobe was a primary carcinoma of the liver. Metastases of the sarcoma occured on the peritoneum, lung, aorta and peribronchial lymph nodes. No metastases of the carcinoma was found. The possibility that cirrhosis may have played a predisposing role in the formation of hepatoma and sarcoma was discussed.

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