Objective: to reveal gender differences in brain structural changes after clinical death and to assess the neuroprotective properties of the hormonal agent Gynodian Depot. Materials and methods. The brain neuronal populations were morphometrical-ly studied in adult albino rats of both sexes which had sustained 10-minute cardiac arrest. At minute 30 after resuscitation, oil solution of estradiol with dehydroepiandrosterone was intramuscularly injected into the study group animals in doses of 0.1 and 5 mg/100 g. The comparison group of animals received the equivalent volumes of saline. Gender- and age-matched intact rats served as a control. An image analysis system of cresyl violet-stained paraffin brain sections was used to determine the density and composition of highly ischemia-perfusion-sensitive populations of pyramidal neurons of Layer V of the sensomo-tor cortex, the CA1 and CA4 hippocampal sectors, and Purkinje cells in the lateral cerebellum. Results. It has been established that there are gender differences in brain morphology in health, which are detectable in the postresuscitative period. The site of lesions has been found to be different in resuscitated rats of different gender. At the same time, male brain lesions are more extensive, i.e. these involve to this or that extent all the examined regions: the cerebellum and CA4 hippocamplal sector exhibit neuronal death; the cortex and CA1 hippocampal sector show dystrophic changes in the nerve cells. In the females, neuronal shedding processes were observed in the CA1 hippocampal sector only. Estradiol + dehydroepiandrosterone treatment has been ascertained to prevent nerve cell death only in the males and to fail to affect the density and composition of the neuronal populations under study in the females. Conclusion. The findings suggest that it is important to identify the structural bases of sexual dimorphism in the body’s reaction to ischemic exposure and that it is necessary to take them into account when developing effective therapy and choosing the optimal treatment policy to correct posthypoxic encephalopathies. Key words: gender differences, postresuscitative neuronal changes, hormonal therapy, morphometry.

The paper deals with Academician V. A. Negovsky’s views of the significance of the central nervous system in the formation of postresuscitative pathology and with the development of this problem at the present time. It also gives Academician V. A. Negovsky’s statements on the most important matters of reanimatology. The authors present the current studies of V. A. Negovsky’s disciples, the researchers of the Institute founded by him, which deal with the regularities of and the mechanisms responsible for the development of posthypoxic encephalopathies. Under discussion are the problems associated with the time course of changes in the postresuscitative process, the impact of the duration of a terminal condition on brain damage, the significance of structure-function relationships, the selective vulnerability of different regions of the central nervous system, the role of the body’s individual and typological characteristics, as well as the methodological approaches to preventing and treating brain dysfunction. Key words: V. A. Negovsky, postresuscitative brain pathology, neuromorphology, regularities and mechanisms of the development of posthypoxic encephalopathies.

The impact of 12-minute clinical death on congenital and acquired behaviors, the content of biogenic amines, the composition and size of neuronal populations in some regions of the albino rat brain were studied. It was shown that there were postresuscitative changes in emotional responsiveness and position-finding and explorative reactions and impairments in learning and memory processes, and decreases in physical endurance and algesthesia. These processes were associated with the changes in the levels of serotonin and noradrenalin in the frontal cortex of the brain, in those of dopamine and serotonin in the striatum, in some plasma biochemical parameters, and loss of neurons in the sector CA1 of the hippocampus and in the lateral sector of the cerebellum.