Медицинская иммунология (Jul 2014)
ENDOTHELIAL DYSFUNCTION AND “OXIDATIVE STRESS” BY THE NONNSTABLE COURSE OF ISCHEMIC HEART DISEASE
Abstract
Abstract. The purpose of study was to compare phagocytic indexes, free oxygen radicals generation, activity of antioxidative protection, cytokine levels and von Willebrand factor (vWF) antigen in the patients with non–stable course of ischemic heart disease of. We examined 58 patients with ischemic heart disease: 31 with unstable angina and 27 with acute myocardial infarction. The methods of study included nitro–blue tetrasolium reduction test for neutrophiles and monocytes, detection of myeloperoxidase in phagocytes, assays of glutatione reductase in neutrophiles, as well as measurements of catalase, superoxide dismutase, malonic dialdehyde, circulating immune complexes, IL–6, TNFα and vWF factor antigen in blood. Upon admission to the hospital, the patients with unstable angina, as well as with acute myocardial infarction showed significantly higher levels of vWF, C–reactive protein, neutrophile myeloperoxidase and appropriate trends in circulating immune complexes, IL–6 and TNFα. In the patients admitted to the hospital with ischemic heart disease with repeated coronary events during the last year of follow–up, as well as in acute myocardial infarction, the levels of vWF antigen were found to be significantly increased. The raise of vWF was accompanied by increased levels of malonic dialdehyde, C3R–induced generation of free oxygen radicals in the neutrophils, and drop in glutatione reductase activity, thus reflecting an “oxidative stress” condition. These patients did also exhibit higher levels of C–reactive protein, circulating immune complexes, IL–6 and TNFα. According to regression analysis data, the levels of vWF antigen and C3R–induced activation free oxygen radicals in neutrophils are the indices that were most closely connected to ischemic heart failure disease within a year of observation. The results obtained point to the important role of “oxidative stress” in the development of endothelial dysfunction in the patients with non–stable course of ischemic heart disease. (Med. Immunol., 2005, vol.7, № 5–6, pp. 569–574)
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