Aim. To study the nature of reactive changes in astrocytic glia and oxidative metabolic status in the visual cortex of experimental animals after acute circulatory arrest. Methods. A series of experiments was performed on 47 mature males of noninbred white rats weighing 150-180 g. Under general ethereal anesthesia, a 5-minute anoxia was modelled by intrathoracic clamping of the vascular bundle of the heart followed by resuscitation and observation of the general state dynamics of the animals within 5 weeks after revitalization. Morphometric characteristics of reactive astrogliosis were studied with evaluation of a neurospecific protein (glial fibrillary acidic protein) by immunohistochemistry. The processes of free radical oxidation in brain homogenates were evaluated by determination of products reacting with thiobarbituric acid and by chemiluminescence analysis. The state of antioxidant system in the studied tissues was determined by recording the activity of superoxide dismutase and the level of reduced glutathione. Results. Regarding astroglial link, significant expression of glial fibrillar acidic protein was recorded throughout the observation period with maximum intensification on day 21 of the experiment. In the early periods and during the second week after recovery, the increase of the light sum of iron-induced chemiluminescence was noted, followed by a prolonged accumulation of secondary metabolites of lipid peroxidation. The investigated level of superoxide dismutase significantly increased not only on days 1-3, but also during the second week of the postresuscitation period. When assessing the level of reduced glutathione, a significant increase of its content occured during the first three days after recovery. Conclusion. The revealed activation of a neurospecific protein production with preceding shifts in pro- and antioxidative systems is indicative of hyperreactive character of astrogliosis formed in brain structures against the continuous oxidative stress, disrupting the functioning of neural networks in the visual cortex of experimental animals.

казанский медицинский журнал, 2015 г., том 96, №5Синдром эндогенной интоксикации в большей или меньшей степени сопутствует любому соматическому, инфекционному, хи-рургическому и другим заболеваниям [5,7].Известны отдельные биохимические механизмы эндотоксикоза, важными из УДК 612.015.11: 612.084: 617.7-005.4: 616.15 РЕпЕРФуЗИОННОЕ ЭНдОтОксИНОВОЕ пОВРЕждЕНИЕ ОРГАНА ЗРЕНИя В ЭкспЕРИМЕНтЕ Методы. Проведены хронические (5 нед) патофизиологические эксперименты на 72 нелинейных половозре-лых крысах-самцах с моделированием острой остановки кровообращения путём пережатия сосудисто-нервного пучка сердца с последующим проведением комплекса реанимационных мероприятий. Уровень эндогенной ин-токсикации оценивали по интегральному индексу эндогенной интоксикации с определением олигопептидов и веществ низкой и средней молекулярной массы, свободнорадикальное окисление в тканях глазного яблока -путём определения продуктов, реагирующих с 2'-тиобарбитуровой кислотой, а также методом хемилюминесцент-ного анализа. Состояние антиоксидантной системы исследовали по характеру каталазной активности и уровню восстановленного глутатиона.Результаты. Выявлено статистически значимое двухфазное нарастание индекса эндогенной интоксика-ции на протяжении всего постреанимационного периода. В тканях глазного яблока отмечено повышение Fe 2+ -индуцированной хемилюминесценции с последующим накоплением вторичных метаболитов перекисного окис-ления липидов, а также усиление активности каталазной системы защиты в ранние сроки (в 1-3-и сутки) и на 2-й неделе. Выявлена положительная корреляция интегрального индекса эндогенной интоксикации с уровнем продуктов, реагирующих с 2'-тиобарбитуровой кислотой в 1-е сутки постреанимационного периода.Вывод. После острой остановки кровообращения происходит формирование синдрома эндогенной интоксика-ции с максимальным накоплением токсических молекул в системном кровотоке на 1-3-и и 10-14-е сутки постре-анимационного периода и выраженной интенсификацией процессов перекисного окисления липидов в тканях глазного яблока в аналогичные сроки наблюдения.ключевые слова: глазное яблоко, реперфузия, перекисное окисление липидов, токсические молекулы, эндо-генная интоксикация. Republican Heart Center, Ufa, Russia Aim. To evaluate the level of endogenous intoxication in the blood and the status of the lipid peroxidation processes in eye tissues of experimental animals after acute circulatory arrest. REPERFUSION ENDOTOXIN EYE DAMAGE IN EXPERIMENTAL STUDYMethods. Chronic (5 weeks) pathophysiological experiments were performed in 72 nonlinear mature male rats, in which acute circulatory arrest was modeled by neurovascular heart bundle compression, followed by resuscitation. Endogenous intoxication intensity was assessed using endogenous intoxication integral index based on the detection of oligopeptides and low and medium molecular weight substances. Free radical oxidation in eye tissues was assessed by determining the level of 2'-thiobarbituric acid-reactive products, as well as by chemiluminescence. The condition of antioxidant sy...

Aim. To assess the influence of the pathogenetic action of the succinate-containing drug on corticosteroid regulation in the kidney of rats with different resistance to hypoxia during recovery after systemic circulation arrest. Methods. The object of the study was male non-inbred white rats weighing 200220 g. A week after testing for resistance to hypoxia, a 5-minute systemic circulation arrest was simulated by intrathoracic clamping of the vascular bundle of the heart, followed by resuscitation. In the postresuscitation period, the experimental rats were once daily injected with a solution containing inosine + nicotinamide + riboflavin + succinic acid, and the control rats 0.9% Sodium Chloride solution. The observation period was 35 days. We studied the content of corticosterone, aldosterone in blood plasma, gluco- and mineralocorticoid receptors, carbonylated proteins, dityrosine, and products that react with thiobarbituric acid in homogenates of the kidneys. Statistical data were presented as mean and standard deviation M. Nonparametric KruskalWallis (N) and MannWhitney (U) tests followed by Dunn test, Spearman correlation analysis were used. Differences were considered statistically significant at p 0.05. Results. The use of succinate-containing preparation reduced the intensity of free radical processes in both groups of animals. Against this background, in low-resistance rats, on the 1st day, the concentration of glucocorticoid receptors statistically significantly increased to 117% (p 0.05), and then was comparable to the control; the greatest statistically significant changes in the level of mineralocorticoid receptors occurred on the 1st day (increase by 25%, p 0.001) and at 2135th days (decrease by 2230%, p 0.001). In highly resistant rats, the correction led to a shift in the maximum content of glucocorticoid receptors from the last day (134% of the control level, p 0.01 without therapy) to the 1st (123%, p 0.05 with succinate-containing therapy) and maintaining the receptors level comparable to the initial, in the future. The level of mineralocorticoid receptors in highly resistant rats was lower than in low resistant rats, both in the group without correction and with correction. Conclusion. Correction of the course of the postresuscitation period with a succinate-containing drug in animals with a low resistance to hypoxia against the background of a decrease in the intensity of carbonyl stress and restoration of feedback mechanisms causes stabilization of glucocorticoid receptors level and a decrease in mineralocorticoid receptors to control values by the end of the experiment; in organisms highly resistant to hypoxia, against the background of correction, the activity of lipid peroxidation decreases and the level of both types of receptors are restored.

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