The volume of hepatic blood flow was determined on a total of 100 hepatic diseass patients; acute hepatitis 2, chronic hepatitis 75, hepatocirrhosis 21 and fatty liver 2; by Galactose continual Infusion Method devised by Nakamura et al. At the same time, the correlation between state of hepatic circulation and BSP test was observed stochastically using as index the BSP test findings noted at time of initial out-patient examination and the BSP test find ings obtained within one week both prior to and after hepatic blood flow volume determination made following admission to the hospital. Further, comparisons were made with the hepatic tissue picture obtained by biopsy. The followresults were obtained.
1) The average value of the total hepatic blood flow Volume for the 100 hepatic disease cases was 857±46 cc/min/M². The 49 cases with wedded hepatic venous pressure (WHVP), but without hepatic shunt flow had an average value of 135±21 mm H₂O.
2) A positive correlation with a coefficient of 0.69 was noted between WHVP and BSP test results. Further, an approximate value of 0.64 was demonstrated between the initial out-patient BSP test findings. In cases with WHVP of over 175mm H₂O, the change-over rate to negative BSP test results following 3 to 4 weeks of hospitalization, bedrest and treatment was 13.8%, and 71.1% for those with values of less than 175mm H₂O.
3) A negative correlation with a coefficient of -0.34 was noted between effective hepatic blood flow volume and BSP test results. Further, a negative correlation of -0.27 was demonstrated between the initial out-patient BSP test findings. In cases with an effective hepatic blood flow volume of less than 500 cc/min/M², the change-over rate to negative BSP test results following 3 to 4 weeks of hospitalization, bedrest and treatment was 35.0%, while that of cases with volumes of over 500 cc/min/M² was 48.9%.
4) A positive correlation with a coefficient of 0.55 was noted between rate of hepatic short circuit and BSP test results. A positive correlation of 0.50 was demonstrated between the initial outpatient BSP test findings. In cases with hepatic short circuit, the change-over rate to negative BSP test results following 3 to 4 weeks of hospitalization, bedrest and treatment was 1%, while that in those without hepatic short circuit was 63.3%.
5) Of the 42 cases with more than a moderate degree of hepatic cell degeneration and necrosis (includes 2 cases with negative BSP test findings from the beginning), 9 cases or 22.5% demonstrated normal BSP test findings following 3 to 4 weeks of hospitalization, bedrest and treatment, while of 58 cases with slight degeneration and necrosis (includes 2 cases with normal BSP test findings from the beginning), 24 cases or 82.8% became normal during the same short period of time.
6) A follow-up BSP test survey wase conducted on 30 chronic hepatitis cases whose BSP test findings at time of discharge had become normal, and aggravations were noted in 11. Among those with aggravations, 7 or 63.5% had hepatic circulatory abnormalities during hospitalization.
7) From the above findings, it has been shown that not only degeneration and necrosis of hepatic cells are related to the BSP test value, but a relationship is also noted between the state of hepatic circulation. Therefore, it is necessary to consider both together before making any decision.

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The Calactose Continual Infusion Method devised by Nakamura et al and the BSP Continual Infusion Method reported by Bradley et al were used simultaneously on 21 chronic hepatitis and 9 hepatocirrhosis patients, and the hepatic blood flow volume was determined. The results obtained are as follows.
1) The total hepatic blood flow volume as determined by both methods were in agreement in cases with comparatively mild hepatic disturbance, but in such cases as hepatocirrhosis where abvanced cellular degeneration and necrosis were present, the value as determined by BSP method was greater than that obtained by the Galactose method. This is felt to be due to BSP clearance, particularly, the close relationship with the hepatic cell uptake capacity of BSP.
2) There is a definite difference in galactose and BSP elimination rates. The 15 cases that demonstrated a 100% elimination of galactose had BSP elimination rates which ranged from 33.0 to 84.6%, thus, in all cases the rates for the latter were lower. From these reslts, even though the BSP method may indicate a normal liver, it is felt that there may be a hepatic shunt blood flow volume, but this is presumed to be due to the fact that the BSP up take capacity of hepatic cells is not 100% or it may be that although they have such uptake capacity, the BSP which has been taken up is again released into the blood.
3) With the use of dogs BSP in amounts less than the Maximum elimination volume of the liver was administered in succession into the peripheral vein, hepatic vein and portal vein by continual infusion, and the BSP concentration in hepatic venous blood was determined. Results showed that both the portal and hepatic venous areas were involved in the hepatic eimination of BSP.
4) Therefore, it is felt inappropriate to use BSP to determine hepatic blood flow volume in cases with hepatic disturbances.

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The concentrations of pyruvate and related compounds in the liver and blood in the recovery of carbontetrachloride intoxication of rats were measured and the effects of pantethine, ATP and DPN administrations were studied.
(1) In the recovery stage from acute carbontetrachloride intoxication, the first and fourth weeks after single subcutaneous administration of carbontetrachloride, and in the recovery stage from chronic carbontetrachloride intoxication, the second and fourth weeks after subcutaneous injection of carbontetrachloride twice a week for four weeks, serum transaminase activities (S GOT and S GPT) returned normal and the histological changes of liver (heamatoxylin-eosin staining) were also normal except for slight irregular cellular ridges and cytoplasmic basophilia.
(2) Decreased pyruvate oxidation in the rat liver mitochondria was still present even though no significant histological changes could be demonstrated microscopically. This might mean that the function of mitochondrial enzymes would not be restored in a shorter time. In the first and fourth weeks of recovery from the acute intoxication, increases of the lactate/pyruvate ratio of the liver were observed. The pyruvate level in the liver did not show any significant change in the recovery from acute and chronic intoxications.
(3) Intraperitoneal administration of pantethine (Bis (N-pantotenyl -ß aminoethyl) disulfide), a precursor of coenzyme A, to carbontetrachloride-intoxicated rats arrested the progression of fibrosis and the formation of pseudoacinus of the liver. The diffuse fatty infiltration of the liver, however, was not prevented by pantethine. The fact that no improvement of the pyruvate-oxidizing activity (QO₂) of liver mitochondria, a decrease of pyruvate level and an increase of cholesterol in the blood were observed with pantethine seems to suggest that the diffuse fatty infiltration of the liver by pantethine might be resulting from decreases of hepatic ATP level and -SH enzyme activities, which would be caused by pantethine administration. Pantethine improved other routine liver fanction tests except for Zinc sulfate test.
(4) Simultaneous administration of pantethine and ATP reduced the extent of diffuse fatty infiltration of the liver. The blood sugar decreased by pantethine and ATP more than by pantethine alone probably due to an insulin like activity of ATP. The blood cholesterol increased, and QO₂ and other routine liver function tests were improved more by pantethine and ATP than by pantethine alone.
(5) Intraperitoneal administration of DPN to carbontetrachloride-intoxicated rats resulted in marked improvements in liver histology, QO₂, lactate/pyruvate ratio of the liver and the other liver function tests.
These results seem to suggest that the progression of the liver injury by carbontetrachloride depends largely on DPN contents.

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