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Shifting extra uterine existence is a serious test of maturity of all functional systems of the newborn, so in recent years, the more attention is payed for the adaptation of the newborn. It is known that the pathological course of pregnancy is a violation of the functional state of the adrenal cortex, and prolonged exposure of the pathological factor leads to the inhibition of adrenocortical function and a decrease of the adaptive capabilities of a newborn. Therefore, serum cortisol levels could be a predictor of complications in preterm infants. Based on this, it seems appropriate to study changes in the content of serum cortisol cord blood prior to the development of various syndromes neonatal maladjustment. The clinical and laboratory examination of term infants with various disorders of adaptation: regurgitation, pain, hyperexcitability , depression, cardio-respiratory depression, bleeding in the skin, toxic erythema. It is shown that the most prominent violations maladjustment processes occur on the background of decreased cortisol. Border states, which are formed on the background of normal or elevated cortisol, are not accompanied by significant impairments of adaptation processes. On the basis of the data was drawn a conclusion about the possibility of using changes of cortisol in cord blood as a reliable indicator of neonatal adaptation processes, pointing to the possibility of the development of pathological conditions.

The article deals with the prospective complex approach to laboratory analysis of energetic metabolism under states of newborns. The approach provides simultaneous detection of content of main energy substrates, activity of adenosinetriphosphatases and succinate dehydrogenases in umbilical blood, characterized by high sensitivity to hypoxia.

Early adaptation issues of newborn rats of Wistar population and August line were examined. Absence of the connection between the condition of a female during the pregnancy and the birth, and newborn rats in early postnatal period was revealed.

24-hour hypokinetic stress expressed in decrease of sensitivity of cellular and humoral immu nity to subsequent immunization with sheep erythrocytes was studied. The development of this phenomenon is associated with sensitization of lymphoid tissue to hypoplasia effect of glycocorticoid hormones. In introduction of glycocorticoid stress, the animals revealed a more pronounced depression of proliferative activity of thymocytes compared with non stressed animals.

For early diagnosis of neonatal transient conditions that may become abnormal, it is promising to apply an integrative approach comprising the concurrent definition of the indices characterized by a high sensitivity to hypoxia. This study has investigated the predictive value of platelet monoamine oxidase and red blood cell Mg-ATPase in neonatal infants.

It was proved that hypoxia tolerance often goes together with forming of oxidative stress tolerance and has genetic predetermination on hypoxic influence. Interline difference ofhypoxia sensitivity is mainly defined by difference of oxygen-transport systems state. Genetically predetermined differences between investigated lines give the August rats the ability to use mechanisms of resistant strategy more effectively, and the Wistar rats--to use tolerant strategy more effectively.

The reactions reflecting adaptation may assume pathological traits under certain conditions. It is necessary to have reliable predictors that characterize adaptive processes. As this criterion, it is expedient to use the most important marker of free radical oxidation, such as xanthine oxidase (XO) activity. On the basis of the authors' findings, it can be said that it is advisable to apply this test to the screening of the course of adaptation within the first days after birth and to the detection of neonatal infants who require more scrupulous attention.

Rarely repeated episodes of immobilization stress led to misbalance between pro oxidant and antioxidant systems. So in the brain, kidneys, spleen we observed elevation of oxidized proteins level. In contrast, in the thymus and bone marrow the protein carbonilation was attenuated. In the liver, oxidized protein level remained unchanged. Simultaneously the level of liver lipoperoxidation was increased. These shifts were accompanied with attenuation of catalase activity in the liver and elevation of xanthine oxidase activity in the spleen and erythrocytes.

Repeated stress led to antipodal directions in immune system and cytochrome P450 activities of normotensive and hypertensive rats. Enhancement of the Reaction of Delayed Hypersensitivity, suppression of cytochrome P450-mediated monooxigenase activities were observed in Wistar rats. On the contrary, in the NISAG decrease of the Reaction Delayed Hypersensitivity, elevation of cytochrome P450-mediated monooxigenase activities were observed, as comparison with Wistar rats.

4 episodes of immobilization stress (60 minutes, once 72 hours) led to diminution of hypoxia tolerance and anxiety-depressive disorders of behavior. The later shifts were associated with decrease of IL-4 concentration and simultaneous increase of IL-6 level in blood serum. The stress-induced behavioral shifts appeared to correlate with IL-4 concentration in blood of stress-sustained rats.

The effect of triamcinolone acetonide (2 mg/kg) on the distribution of morphologically mature leukocytes in the blood system, the mononuclear liver infiltration, and the immune response was studied in rats under conditions of stress-induced hypoxia. Administered under these conditions, the drug produces a less pronounced effect on the content of circulating lymphocytes, the lymphoid cell number in the bone marrow, and the number of hepatocytes and monocytes/macrophages in the liver. However, the post-stressor immunodepressant effect of triamcinolone acetonide was increased and accompanied by the development of hepatic damage.

4 episodes of immobilization stress caused anxious and depressive behavioral disorder in rats, accompanied by decreased sensitivity of pancreatic tissue to alloxan-induced damage, and simultaneously increased sensitivity of hepatic tissue to alloxanogenic inflammatory effect. The latter shifts were accompanied by a more pronounced hyperglycemia. The paper discusses a probable role of hepatitis in hyperglycemic response to alloxan challenge associated with stressogenic anxiety.