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    Online-Ressource
    Online-Ressource
    ECO-Vector LLC ; 2013
    In:  Kazan medical journal Vol. 94, No. 5 ( 2013-10-15), p. 723-726
    In: Kazan medical journal, ECO-Vector LLC, Vol. 94, No. 5 ( 2013-10-15), p. 723-726
    Kurzfassung: Aim. To study the features of inflammatory effector mechanisms variation in Wistar rats with metabolic non-coronary myocardial infarction. Methods. Metabolic myocardial infarction was reproduced in Wistar rats by adrenalin injection. Metabolic myocardial infarction was verified by electrocardiography and histological examination. Biocidal activity of blood neutrophils was determined by nitro blue tetrazolium test and chemiluminescence, cytokine serum levels (interleukin-1β, interleukin 6 and tumor necrosis factor alpha) were determined by ELISA. Lipid peroxidation was assessed by measuring malondialdehyde, diene conjugates and diketones blood concentrations. Catalase activity and reduced glutathione level were determined in erythrocyte hemolysate, serum activity of superoxide dismutase was also measured. Intact animals were examined as a control group. Results. In rats with metabolic myocardial infarction, oxygen-dependent leukocyte biocidity (determined by nitro blue tetrazolium test and chemiluminescence) increased dramatically from the first day of the adrenalin administration and continued to increase until the end of the experiment (day 14). Accordingly, the production of active oxygen metabolites, which intensified the lipid peroxidation, was increasing. Simultaneously an imbalance between pro-and antioxidant system parameters was detected. Serum concentration of pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin-1β, interleukin-6) increased. Conclusion. Long-term administration of adrenalin to experimental animals causes an increase in the neutrophils biocidal activity, accompanied by release of reactive oxygen species, pro-inflammatory cytokines, lipid peroxidation intensifying and decreased compensation by antioxidant defense system, which together can be a powerful trigger of myocardial damage.
    Materialart: Online-Ressource
    ISSN: 2587-9359 , 0368-4814
    URL: Issue
    Sprache: Unbekannt
    Verlag: ECO-Vector LLC
    Publikationsdatum: 2013
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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