Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • creatinkinase activity  (1)
  • deflazacort  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 45 (1993), S. S17 
    ISSN: 1432-1041
    Keywords: Basophils ; Cyclosporin A ; Corticosteroids ; deflazacort ; histamine ; leukotriene C4
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Pro-inflammatory and vasoactive mediators released from human basophils and mast cells play a role in several inflammatory and immune disorders. It was recently demonstrated that cyclosporin A (CsA) exerts anti-inflammatory effects by inhibiting the release of preformed and de novo synthesized mediators from human basophils [1]. This study compared the effects of pharmacological concentrations of deflazacort (DFZ) and prednisolone (PRED) on the anti-IgE-mediated release of preformed (histamine) and de novo synthesized (leukotriene C4: [LTC4]) mediators from basophils. Basophils were cultured for 18 hours in the presence of pharmacological concentrations of DFZ (10−8 to 3 × 10−6 M). DFZ inhibited the anti-IgE-mediated release of histamine and LTC4 from basophils in a concentration-dependent manner (6–40 %), and had a similar efficacy and potency to PRED. The effect of DFZ (10−8 to 10−8 M) in combination with CsA on the immunological release of histamine and LTC4 from basophils was also evaluated. An 18-hour incubation of basophils with DFZ (10−8 M) followed by a short (15-minute) incubation with CsA (30 ng/ml) resulted in an additive inhibition of the release of histamine and LTC4. The additive anti-inflammatory effect of these drugs makes them interesting candidates for future controlled clinical trials in inflammatory diseases in which basophil-derived mediators play a relevant role.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 78 (1983), S. 289-297 
    ISSN: 1435-1803
    Keywords: tyramine ; myocardial lesions ; myocardial ultrastructure ; creatinkinase isoenzyme ; creatinkinase activity ; Sprague-Dawley rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The authors performed an experimental study on myocardial injury induced by tyramine. For this purpose Sprague-Dawley male rats received multiple dose levels of tyramine hydrochloride. The drug exerts its sympathomimetic effects chiefly by the release of catecholamines stored in nerve endings. Myocardial lesions were documented on the basis of serum creatinkinase isoenzyme (MB-CK) changes and creatinkinase activity (CK) depletion in homogenate of cardiac tissue in animals sacrificed at different time intervals from tyramine injection. Accordingly, MB-CK values expressed as IU/l×103 (mean±standard error of the mean, [SEM]) assessed at the 2nd and 4th hours from 50, 100, or 150 mg i.p. tyramine/100 g body weight were 0.99±0.23 or 0.85±0.30 (50 mg), 1.75±0.24 or 8.50±0.41 (100 mg), 2.07±0.60 or 8.40±0.39 (150 mg), respectively. Values in control animals were 0.51±0.07. As shown, the most marked increase in MB-CK levels is obtained at the 4th hour in 100 mg/100 g b.w. tyramine-treated rats. Thus MB-CK values were also explored at the 6th (7.43±0.15) and 12th (2.24±0.23) hours from drug administration. A significant (p〈0.001) rise in serum MB-CK levels can be observed reaching the peak at the 4th hour after tyramine (100 mg/100 g b.w.). Moreover, the CK myocardial content (IU/mg of protein) in the same tyramine-animals at the 2nd or 4th hours from 50, 100 or 150 mg of the i.p. drug/100 g b.w. were (mean ± SEM) 11.10±0.05 or 9.26±0.57 (50 mg), 9.42±0.81 or 8.57±0.22 (100 mg), 8.92±2.17 or 6.70±0.04 (150 mg), respectively. At the 6th or 12th hours from i.p. tyramine (100 mg/100 g b.w.) CK values were 9.60±0.48 or 9.99±0.56. Control values showed 13.50±0.68. A significant (p〈0.001) decrease in CK myocardial content in the rats treated by the drug was achieved with the most marked CK depletion 4 hours after receiving tyramine (100 mg/100 g b.w.). On these bases, the ultrastructural changes were investigated in tyramine-treated rats (100 mg/100 g b.w.) at the 4th hours from the drug administration. The finding included mitochondrial and myofibrillar damage. In conclusion, this experimental model accounts for the possibility to induce myocardial damagein vivo in tyramine-treated rats.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...