The review article deals with the problem of ischemic preconditioning, the universal physiological mechanism of cell protection from hypoxia. Preconditioning is the term used to describe a phenomenon of the enhanced tolerance of a cell to a damaging factor due to its preliminary effects of stressful stimuli. The article describes the phenomenon of ischemic preconditioning and summarizes the results of a study of the possible mechanisms of this effect in organs and tissues. It discusses the key role of the enzyme glycogen synthase 3fl in the regulation of the mitochondrial pore and that of the latter in the protection of a cell from hypoxia. Experimental data are given on the testing of different drugs as pharmacological agents that initiate/inhibit preconditioning. Reasons for the selective efficacy of some antihypoxants and antioxidants are analyzed in the context of the ischemic preconditioning theory. Conventional anesthetics and analgesics as potential inductors or inhibitors of the process in question are discussed. Key words: ischemic preconditioning, hypoxia, anesthetics, cyto-protection.

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.