Biomedical subjects
Publications and source records attributed to J Nishikawa.
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Lobar attenuation difference of the liver was demonstrated by computed tomography (CT) in 16 cases among over 1,000 cases in which CT scans of the liver were obtained. Cases were divided into two groups: with liver tumor and without liver tumor. Among the former group, hepatocellular carcinomas is the predominant lesion; tumor thrombus in the portal vein is presumably the cause of the attenuation difference. The latter group includes the patients with hepatocellular disease and clinically normal patients. In the former group, the tumor itself could not be noted in precontrast scans in eight out of 12 cases. When lobar attenuation difference of the liver is noted, a postcontrast scan should be obtained to determined whether there is a liver tumor in the lobe of lower attenuation.
The oral acute toxicity of 3 beta-adrenoceptor stimulants, 2 beta-adrenoceptor blockers, and 2 anti-gastric ulcer drugs was studied in 8-week old, SD-JCL rats and ICR-JCL mice, fasted overnight for 17-20 hours. The results were compared with those from rats and mice allowed to feed normally. The order of the fed:fasted ratio of LD50 values in rats was pirenzepin less than propantheline less than pindolol less than salbutamol less than orciprenaline less than fenoterol less than bunitrolol, and was in the range 1.3-4.7. The increased toxicity in fasted animals was considered to be related to acceleration in gastric emptying and intestinal absorption, but not to a general change in the condition of the test system or a decrease in the detoxification ability of the liver because after intraperitoneal administration acute toxicity was similar in fed and fasted rats.
Acute oral toxicity of the three Beta-adrenoceptor stimulants Orciprenalin, Fenoterol and Salbutamol as well as the two Beta-adrenoceptor blockers Pindolol and Bunitrolol was studied in singly-housed and aggregated male and female mice (ICR-JCL) and the results were compared with those in grouped mice (background studies). With a few exceptions, the acute toxic potency of the five test substances in mice appeared to be: Aggregated mice greater than grouped mice greater than singly-housed mice.
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Radionuclide Computed Tomography (RCT) was performed in 40 cases with various liver diseases. Indication of RCT was determined by the fact that usual liver scintigrams showed or suspected space-occupying lesion. In diffuse hepatocellular disease, RCT added diagnostic informations in 10 out of 17 cases. In these patients, RCT referred decreased uptake area to morphological change such as prominent porta hepatis, widening of both lobes or lateral seg. and medial seg, of the left lobe, and so on. In cases with liver tumor, RCT demonstrated the liver by axial plane, so one could easily or precisely diagnose the location of the mass. RCT performance requires only 30 min, additionally, and no additional injection. We conclude RCT should be performed to the patients whose liver scintigrams show or suspect space-occupying lesion.
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The effect of sodium picosulfate was examined in liver cell cultures of rabbit, rat and man exposed to substance concentrations of 25, 50, 100, 200, 400, 800 and 1600 micrograms/ml. At 400, 800 and 1600 micrograms/ml the rapidly growing cultured liver cells of rabbit showed dose-dependently vacuolic and fatty change as well as necrosis combined with a lowered mitotic activity and a slight increase in LDH values in the medium at 800 and 1600 micrograms/ml. Comparable but less severe effects were observed in 4-day old liver cell cultures of rat, while liver cells cultured for 6 to 11 days tolerated 1600 micrograms/ml sodium picosulfate. In human liver cultures the number of cells was slightly lowered at 800 and 1600 micrograms/ml and the number of nuclei in division was decreased dependent on dose.
Cultured liver cells of man, rat and rabbit were exposed to sodium picosulfate using medium concentrations of 400, 800,1000,1600, or 2000 micrograms/ml, and the results were compared with findings after bisacodyl at 25, 50 or 100 micrograms/ml and sennoside at 100 or 200 micrograms/ml. Much higher concentrations of sodium picosulfate than of both comparative substances were tolerated. At the doses used, hepatocytes of rabbit were slightly more sensitive against sodium picosulfate, while effects of bisacodyl and sennoside on hepatocytes were comparable between the three species used. No substance-related deviations in leakage of LDH from liver cells into culture medium were observed. The protein content was lowered in liver cells of rabbit exposed to 1600 micrograms/ml sodium picosulfate and the human cells exposed to 100 micrograms/ml bisacodyl. An increase in spindle-shaped growth occurred only in human cells exposed to bisacodyl.
Cytotoxic effects were studied in Chang liver cells exposed to 4,4'-dihydroxy-diphenyl-(2-pyridyl)-methane-bis(hydrogen sulfate) (ether)-disodium salt (sodium picosulfate) and the results were compared with the effects of other laxatives. Sodium picosulfate caused a decrease in cell growth parallel to a decrease in glucose consumption and lactate production at 2000 and 4000 microgram/ml. On the contrary, 4,4'-dihydroxy-diphenyl-(2-pyridyl)-methane (bis-acodyl) decreased cell growth at 25 and 50 microgram/ml, while glucose consumption, lactate production and the molar ratio of glucose converted to lactate were increased. These effects were also observed with 4,4'-dihydroxy-diphenyl-(2-pyridyl)-methane (La 96), 3,3-bis(p-hydroxyphenyl)oxindole (oxyphenisatin acetate) and 3,3-bis(p-acetoxyphenyl) phthalide (phenolphthalein) at doses of 25 and 50 microgram/ml. Diphenolic compounds seem to increase anaerobic glycolysis by inhibition of respiration. This assumption was confirmed with potassium cyanide, which is known to inhibit the electron transport in the respiratory chain. Actinomycin D, cycloheximide and hydroxyurea did not show such effects.
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