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  • 1990-1994  (2)
  • 1991  (2)
Material
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  • 1990-1994  (2)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 32 (1991), S. 213-216 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dantrolene strongly and dose-dependently inhibited histamine release from rat peritoneal mast cells induced by anti-IgE. Dantrolene inhibited Ca2+-mobilization from intracellular Ca2+-store as well as histamine release in mast cells activated by anti-IgE, the effect on both of these phenomena being closely correlated. These results suggested that the effect of dantrolene on histamine release from rat mast cell might be due to the inhibition of Ca2+-release from intracellular Ca2+-store.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A toxic substance (P-II fraction), fractionated from the pedicellariae of the sea urchinToxopneustes pileulus, dose-dependently caused the histamine release from rat peritoneal mast cells. The histamine release induced by P-II fraction increased with time, while compound 48/80 caused a more rapid histamine release. The dose-response curve for P-II fraction was studied with concentration 0.03–2.0 mg/ml. This reaction was dependent on Ca2+ and temperature. When glucose (5.5. mM) was omitted during the incubation step, the histamine release induced by P-II fraction was significantly reduced as compared to that of compound 48/80. Pyruvate reversed this reduction. On the other hand, the histamine release induced by P-II fraction was effectively potentiated by the addition of glucose (11.0 mM), but not that by compound 48/80. These results suggest that P-II fraction-induced histamine release differs from that of compound 48/80 disregards to the effects of glucose, because this histamine release appears to be more sensitive to the glycolytic pathway than compound 48/80-induced histamine release.
    Type of Medium: Electronic Resource
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