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

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.

Effect of hemic hypoxia on dynamics of GFAP concentrations in the structures of the brain and blood serum of rats

This article clarifies the questions on study of hypoxic influence on distribution of filament and soluble forms of GFAP in various structures of the brain (neocortex, cerebellum, hippocampus, striatum, middle brain, pons) and blood of the rats. Quantitative analysis of the contents of GFAP in the brain structures of hypoxic rats has established that hemic hypoxia results in changes in intracellular levels of GFAP forms and also in updating their ratio, which allows one to assume not only a change in astroglial cells, but also testifies to reorganization in the system of intermediate filaments of astrocytes. The level of GFAP substantially changed in all cerebral formations, which was already investigated in the early terms of hypoxic period. Observations showed that hemic hypoxia exerted a varied influence on expression of neurospecific protein in the different structures of cerebrum of rats. Differences in expression of GFAP can be caused by the regional differences in astroglial cellular population, and also their internal features that define the possible answers to hypoxic damage in different functional and morphological structures of the brain. An increase in expression of the investigated form of protein can explain strengthening of astroglial reactivity, a feature of the brain that appears in various types of pathologies of the CNS. Reactive asters in such exhibit hypertrophy and are characterized by an increased level of GFAP, which is an early and reliable indicator of astroglial pathology. An increase in expression of the investigated form of protein may be explained by strengthening of astroglial reactivity, a feature of the brain that appears in various types of pathologies of the CNS. The contents of GFAP in the blood of adult rats, as a result of the hypoxic influence received from it, can indicate a release of GFAP from damaged astrocytes in the blood flow.