Open AccessFeatures of cellular and molecular inflammatory mechanisms involvement in hormone-mediated myocardial experimental injury
Author(s) -
N. N. Mayanskaya,
L. D. Hidirova,
S. D. Mayanskaya
Publication year - 2013
Publication title -
kazanskij medicinskij žurnal
Language(s) - English
Resource type - Journals
eISSN - 2587-9359
pISSN - 0368-4814
DOI - 10.17816/kmj1928
Subject(s) - lipid peroxidation , superoxide dismutase , malondialdehyde , chemistry , reactive oxygen species , medicine , endocrinology , tumor necrosis factor alpha , catalase , interleukin , oxidative stress , pharmacology , antioxidant , myocardial infarction , cytokine , biochemistry
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.