Abstract
The literature review presents current information on the role of oxidative stress in the pathogenesis of cerebral ischemia / reperfusion. In patients with ischemic stroke, activation of enzymatic and non-enzymatic links of antioxidant defense in the form of an increase in the blood and cerebrospinal fluid of the activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, the content of glutathione reflects the presence of compensatory reserves, is a favorable factor for the restoration of brain functions. An increase in the content of markers of lipid peroxidation in various biological environments in patients with strokes, mainly malondialdehyde, even in combination with an increase in the content of markers of antioxidant protection, indicates its insufficiency and an unfavorable prognosis of the disease. An increase in the content of markers of lipid peroxidation, mainly malondialdehyde, in patients with strokes in various biological environments, even in combination with an increase content in markers of antioxidant protection, indicates its insufficiency, an unfavorable prognosis of the disease. The presence of affective disorders and the persistence of residual manifestations of ischemic stroke may be due to permanent oxidative stress. When choosing a therapy aimed at increasing the activity of antioxidant protection and reducing the toxic effect of prooxidants, one should take into account the severity and dynamics of metabolic disorders. In the presence of data reflecting insufficient activity of antioxidant systems in combination with increased activity of prooxidant systems, the appointment of drugs that reduce the severity of oxidative stress in the early stages of stroke is indicated. Therapy including antioxidant drugs is also indicated in patients with post-stroke affective disorders and with residual symptoms of stroke.
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