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  • Title: Redox Regulation of Neutrophils and Monocytes in Different Types of Myocardial Infarction.
    Author: Romanov VA, Kratnov AE, Romanova NV, Patrunov YN.
    Journal: Russ J Immunol; 2000 Dec; 5(4):413-420. PubMed ID: 12687197.
    Abstract:
    The common aspect in pathogenetic mechanism of occurrence of myocardial infarction with presence or absence of pathologic Q-wave on electrocardiogram, is associated with systemic inflammatory process with involvement of activated neutrophils and monocytes, whose increased oxygen radical production may lead to damage of endothelial cells and cardiomyocyte lipid membranes. For neutrophils and monocytes redox regulation study, 58 myocardial infarction patients were examined by means of chemiluminescenne and nitroblue tetrasolium test. Significant increase of phagocyte functional activity in all patients was observed. Substantially higher parameters of neutrophil hydrogen peroxide and hypochloric acid production were revealed in Q-wave myocardial infarction patients. This assumes the prevalence of irreversible lipid peroxidation in cardiomyocytes destruction process because of neutrophil redox metabolism activation. The absence of significant difference in neutrophil superoxide production and plasma superoxide dismutase in both types of myocardial infarction suggests not only the sufficient functional reserve of their membrane NADPH-oxidase, but the presence of an additional source of active oxygen forms, probably associated with xantinoxidase reaction with activated neutrophil protease participation. The evaluated more expressed chemiluminescence activation index in Q-wave myocardial infarction patients reflects the exhaustion of plasma "antiradical potential", associated with the decrease of antioxidant reserve, and creating conditions for uncontrollable lipid peroxidation intensification. Thus, the heterogeneity of redox metabolism of neutrophils and monocytes in non-Q-myocardial infarction and Q-myocardial infarction patients reflects the difference in cardiomyocyte damage mechanisms in both types of ischemic heart disease aggravation.
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