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.
Aim. Study of the relationship between the parameters of free radical oxidation of proteins and lipids in the murine kidneys in the post-resuscitation period after stopping the systemic circulation, depending on their resistance to hypoxia. Methods. The systemic circulation was stopped by intra-thoracic clamping of the neurovascular bundle for 5 minutes, performed under general ether anesthesia in male noninbred white rats, divided after testing into two groups based on resistance to hypoxia. The observation period lasted for 35 days. In the homogenates of kidney tissues, the content of products reactive to tiobarbituric acid, carbonylated proteins, the formation of metal-catalyzed carbonylated proteins and bitirozin were determined. Results. The characteristic manifestation of oxidative stress in the recovery period after stopping blood circulation and resuscitation was found to be reciprocity of the relationship between the levels of lipoperoxidation and oxidative modification of proteins. Highly resistant to hypoxia animals were characterized by high resistance of proteins of kidney tissue to free radical oxidation against the background of high levels of lipid peroxidation. On the contrary, in animals non-resistant to hypoxia, against the background of relatively low values of lipoperoxidation, high levels of oxidative modification of proteins, both initial and induced, were recorded. Conclusion. In post-resuscitation period in highly resistant to hypoxia animals, marked activation of lipoperoxidation occurs accompanied by a transient increase in the carbonylation of proteins in the early observation period; for low-resistant to hypoxia animals high intensity of carbonyl stress against the background of the relative «preservation» of lipid structures of the cell is characteristic, which persists throughout the post-resuscitation period, which can make a significant contribution to kidney damage, increasing the risk of renal failure.
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.
Objective — To assess the antioxidant activity of rat liver after systemic ischemia reperfusion (IRP). Material and Methods — The study was conducted on 70 male rats. For all animals of the treatment group (n=35) under ether anesthesia, we were stopping stopping systemic circulation for five minutes. After that, the animals were given an external cardiac massage and artificial lung ventilation. We did not perform circulatory arrest after ether anesthesia in animals of the control group (n=35). In all animals, we were measuring the levels of serum hormones (corticosterone, aldosterone), the content of glucocorticoid and mineralocorticoid receptors in liver homogenates, and the activity of enzymes of the antioxidant system (superoxide dismutase and catalase). We were making control measurements on days 1, 3, 5, 7, 14, 21, and 35 after the simulated IRP. Results — On day 1 after simulation of IRP development, the levels of cortisol and aldosterone in the serum of treatment group rats were significantly higher, by 14.3% and 33.5%, respectively, compared with the control group. In response to stress (IRP), we observed the highest concentration of cortisol in the blood of treatment group rats on day 3 (p=0.0002), which decreased afterwards. On day 1 after IRP, there was a reduction in the activity of superoxide dismutase and catalase in treatment group rats, by 50.3% and by 29%, respectively (p<0.0001). The lowest antioxidant activity in the rat liver after IRP was observed on days 3-7. Conclusion — Systemic IRP is associated with pronounced changes in the dynamics of corticosteroid receptors in the liver, which leads to a reduction in the activity of key antioxidant enzymes.
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