EFFECTS OF ACTOVEGIN ON THE CENTRAL NERVOUS SYSTEM DURING POSTISCHEMIC PERIOD

In a rat model of 5-min clinical death caused by massive blood loss actovegin prevented the development of metabolic disorders induced by hypoxia and reoxygenation as well as the damage to the central nervous system in the early postresuscitation period. Intracarotid administration of actovegin increased the activity of reduction-oxidation enzymes, intensified aerobic metabolism of glucose, prevented lactate accumulation in the brain, reduced structural disorders in the central nervous system, and provided faster restoration of the major reflexes after a 5-min total ischemia.