SUBCELLULAR DISTRIBUTION OF 3H-DIGITOXIN AND ITS METABOLITES IN THE HEARTS OF THE CATS WITH A HYPERSENSITIVITY TO THE DRUG
To clarify the cause of hypersensitivity to digitoxin, an experiment was carried out with cats. The most potent hypersensitivity to digitoxin has been observed 48 hr after the injection of a loading dose. However, 1 hr after this injection, the cats failed to show the hypersensitivity. One, 24 and 4...
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| Published in | Japanese journal of pharmacology Vol. 33; no. 4; pp. 765 - 773 |
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| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
The Japanese Pharmacological Society
1983
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| Abstract | To clarify the cause of hypersensitivity to digitoxin, an experiment was carried out with cats. The most potent hypersensitivity to digitoxin has been observed 48 hr after the injection of a loading dose. However, 1 hr after this injection, the cats failed to show the hypersensitivity. One, 24 and 48 hr after the injection of 3H-digitoxin, the contents of digitoxin and its metabolites in subcellular fractions of hearts were measured. Digitoxin contents in microsomal fractions 48 hr after the injection only slightly decreased, while those in mitochondrial and nuclear fractions markedly decreased as compared with the check at 1 hr. An increase of sodium ions and a decrease of potassium ions in the hearts were seen 48 hr after the injection. These facts may be related to the cause of hypersensitivity. |
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| AbstractList | To clarify the cause of hypersensitivity to digitoxin, an experiment was carried out with cats. The most potent hypersensitivity to digitoxin has been observed 48 hr after the injection of a loading dose. However, 1 hr after this injection, the cats failed to show the hypersensitivity. One, 24 and 48 hr after the injection of 3H-digitoxin, the contents of digitoxin and its metabolites in subcellular fractions of hearts were measured. Digitoxin contents in microsomal fractions 48 hr after the injection only slightly decreased, while those in mitochondrial and nuclear fractions markedly decreased as compared with the check at 1 hr. An increase of sodium ions and a decrease of potassium ions in the hearts were seen 48 hr after the injection. These facts may be related to the cause of hypersensitivity. |
| Author | FUJINO, Sumiko TSUKADA, Hideki |
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| References | 4) Okita, G.T., Kelsey, F.E., Talso, P.J., Smith, B.S. and Geiling, E.M.K.: Metabolic fate of radio-active digitoxin in human subjects. J. Pharmacol. Exp. Ther. 115, 371-379 (1955 6) Izumi, T.: Studies on the accumulation of digitoxin and the cumulative effect of digitalis. Sapporo Med. J. 43, 273-287 (1974 10) Lee, K.S. and Klaus, W.: The subcellular basis for the mechanism of inotropic action of cardiac glycosides. Pharmacol. Rev. 23, 193-261 (1971 2) Bauer, H.: Zur Kenntnis der Ursachen der Kumulierungserscheinungen der Digitalis-glykoside. Naunyn Schmiedebergs Arch. Pharmacol. 176, 65-76 (1934 18) Dutta, S., Goswami, S., Lindower, J.O. and Marks, B.H.: Subcellular distribution of digoxin-H3 in isolated guinea pig and rat hearts. J. Pharmacol. Exp. Ther. 159, 324-334 (1968 11) Fujino, S. and Fujino, M.: Ouabain potentiation of rapid cooling contracture of caffeinized cardiac muscles in calcium deprived medium. Japan. J. Pharmacol. 30, 711-720 (1980 19) Fujino, S., Kawagishi, S., Eguchi, N. and Tanaka, M.: Binding site of ouabain in cardiac muscle cell and its positive inotropic effect in cat. Japan. J. Pharmacol. 21, 423-424 (1971 20) Stephen, P.M., Dutta, S. and Marks, B.H.: The uptake and subcellular distribution of radio-labeled metabolites of digoxin in the isolated perfused guinea-pig heart. Naunyn Schmiedebergs Arch. Pharmacol. 292, 251-254 (1976 23) Yoshida, Y.: Biliary excretion of digitoxin and its metabolites in cats. Sapporo Med. J. 43, 296-300 (1974 14) Katzung, B.G. and Meyers, F.H.: Biotransformation of digitoxin in the dog. J. Pharmacol. Exp. Ther. 154, 575-580 (1966 16) Akera, T., Larsen, F.S. and Brody, T.M.: The effect of ouabain on sodium- and potassium-activated adenosine triphosphatase from the hearts of several mammalian species. J. Pharmacol. Exp. Ther. 170, 17-26 (1969 13) Fujino, S. and Fujino, M.: Ouabain potentiation and Ca release from sarcoplasmic reticulum in cardiac and skeletal muscle cells. Can. J. Physiol. Pharmacol. 60, 542-555 (1982 7) Matsui, H. and Schwarz, A.: Mechanism of cardiac glycosides inhibition of the (Na+-K+)-dependent ATPase from cardiac tissue. Biochim. Biophys. Acta 151, 655-663 (1968 17) Lewin, E., Charles, G. and McCrimmon, A.: Discharging cortical lesions produced by freezing; the effect of anticonvulsants on sodium-potassium-activated ATPase, sodium, and potassium in cortex. Neurology (N.Y.) 19, 565-569 (1969 5) Izumi, T., Fujino, S., Yorozuya, S. and Tanaka, M.: Accumulation of digitoxin by the heart and the cumulative effect of digitalis. Japan. J. Pharmacol. 18, 269-270 (1968 22) Herrmann, I. and Repke, K.: Species unterschiede in der Biotransformation von Digitoxin. Arch. Exp. Pathol. Pharmak. 247, 35-48 (1964 3) Weese, H. and Dieckhoff. J.: Zur Kumulation der Digitalisglykoside. Naunyn Schmiedebergs Arch. Pharmacol. 176, 274-283 (1934 8) Schwarz, A., Lindenmayer, G.E. and Allen, J.C.: The sodium-potassium adenosine triphosphatase: Pharmacological, physiological and biochemical aspects. Pharmacol. Rev. 27, 3-134 (1975 21) Marzo, A., Chirardi, P., Prett, A., Lombardo, A., Longhini, C. and Musacci, G.: Subcellular distribution of deslanatoside C, ouabain and digitoxin in the heart and liver of conscious guinea pigs. Biochem. Pharmacol. 26, 2427-2431 (1977 1) Gold, H. and Degraff, A.G.: Studies on digitalis in ambulatory cardiac patients. JAMA 92, 1421-1424 (1929 9) Fujino, S., Tanaka, M. and Fujino, M.: Micro-injection of ouabain into crab muscle fibers. Nature 223, 413-414 (1969 12) Fujino, S., Igarashi, T. and Hoshi, K.: Ouabain potentiation of Ca release from fragmented cardiac sarcoplasmic reticulum from isolated cat heart. Experientia 35, 1220-1221 (1979 15) Lowry, O.H., Rosebrough, N.J., Farr, A.L. and Randall, R.J.: Protein measurement with the Folin phenol reagent. J. Biol. Chem. 193, 265-275 (1951 |
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