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It has been shown autoradiographically using 3H-lysine-3H-glycin mixture that acute hypoxic hypoxia leading to mass diffuse dystrophy of brain cortex neurons in rats causes a statistically significant decrease in the level of protein synthesis in cortical neurons. The biochemical study of the same material using 3H-leucine has demonstrated that the overall level of protein synthesis in the total cortical tissue (in nerve and non-nerve cells) is not reduced after hypoxia probably due to a high resistance of glial and other non-nerve cells to oxygen deficiency. Transplantation of embryonic nervous tissue into the brain of rats exposed to hypoxia results not only in normalization of the structure of a part of dystrophic neurons but also in a statistically significant increase in the level of protein synthesis which is retained up to the end of the experiment (i. e. for 120 days following the operation) in the total cortical tissue and reaches the normal value in neurons as established autoradiographically.

The aim of this work was to study the effect of hypoxia on blood-brain barrier (BBB) permeability to blood globulins in adult Wistar rats; the influence of hypoxia combined with embryonic nervous tissue (ENT) transplantation; as well as that of hypoxia and brain injury without transplantation. Impairments in BBB were detected by a change in the brain vessels permeability to blood globulins on the basis of Coons's reaction. BBB permeability was checked at different time intervals: from one to thirty five days after the hypoxia seance, hypoxia and brain injury, and hypoxia with ENT transplantation. BBB permeability to blood globulins was found to be significantly increased after the exposure to hypoxia, reaching its maximum by the 7th day and returning to normal only by the 30th day after the hypoxia seance. Similar results were obtained in the case of brain injury following an exposure to hypoxia. Although there was an insignificant decrease in BBB permeability seen one day after the rats were subjected to brain injury, the duration of BBB restoration was the same as in hypoxia-exposed rats (30 days). In the case of ENT transplantation into the brain of adult hypoxia-exposed rats the restoration of the damaged BBB proceeded considerably faster than in hypoxia-exposed rats with brain injury. By the end of the first week after the transplantation the functions of BBB were completely normalized and in some cases the barrier was already restored.

Our early studies (Polezhaev and Alexandrova, 1986) have shown that acute hypoxic hypoxia in rats causes mass (up to 36%) diffuse dystrophy of brain cortex neurons and that after transplantation of embryonic nervous tissue (ENT) into the brain of hypoxia-exposed rats the dystrophy and death of cortical neurons are reduced to 25% due to normalization of a part of dystrophic neurons. In the present work we studied changes in the RNA synthesis in neurons and in the total brain cortex of rats after hypoxia and subsequent transplantation of ENT into their brain by the autoradiographic and biochemical methods using 14C-adenine. It has been shown that under the action of hypoxia the RNA synthesis in neurons and in the total brain cortex of rats is reduced and after transplantation of ENT into the brain of these rats the RNA synthesis is stimulated and normalized both in neurons and in the total brain cortex.