Post-hypoxic reaction of astrocytes of the visual cortex in the experiment

Abstract

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.