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The mechanism by which intravenous administration of nicotinic acid (NA) increases serum unconjugated bilirubin in patients with the Gilbert's syndrome has been investigated. Studies using the technique of percutaneous transhepatic catheterization of the splenic vein and coil planet centrifuge suggested that following intravenous injection of NA some of the circulating erythrocytes were rendered osmotically fragile and trapped by the spleen and that unconjugated bilirubin increased in the splenic vein blood. In patients with liver cirrhosis, the increments of unconjugated bilirubin were closely correlated with the weights of the spleens removed for the management of varices. In rats, intravenous NA injection enhanced heme oxygenase activities in the spleen, but not uridine-5'-diphosphate (UDP)-glucuronyltransferase activity in the liver. These results are consistent with the hypothesis that NA-induced unconjugated hyperbilirubinemia is a result of complex reactions which include increased erythrocyte fragility, increased splenic heme oxygenase activity, and increased formation of bilirubin in the spleen.
H Ohkubo, and
H Musha, and
K Okuda
January 1953,
Acta pharmacologica et toxicologica,
H Ohkubo, and
H Musha, and
K Okuda
January 1960,
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H Ohkubo, and
H Musha, and
K Okuda
August 1960,
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H Ohkubo, and
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K Okuda
May 1952,
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H Ohkubo, and
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K Okuda
February 1957,
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H Ohkubo, and
H Musha, and
K Okuda
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H Ohkubo, and
H Musha, and
K Okuda
January 1986,
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H Ohkubo, and
H Musha, and
K Okuda
January 1965,
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H Ohkubo, and
H Musha, and
K Okuda
June 1956,
Kekkaku : [Tuberculosis],
H Ohkubo, and
H Musha, and
K Okuda
October 1948,
The Journal of biological chemistry,
