Effect of Hypoxic Preconditioning on Stress Reaction in Rats.

In rats, immobilization stress (24 h) induced involution of the thymus and spleen, adrenal hypertrophy, and pronounced elevation (by 67%) of serum cortisol in comparison with intact animals; the mean number of stomach ulcers in rats subjected to stress was 6.9. Hypoxic preconditioning consisting of 6 sessions of 10-min hypoxia (8% O2) followed by 10-min reoxygenation with atmospheric air induced adrenal hypertrophy and spleen involution, but did not change blood cortisol level; no stomach ulcers were found in preconditioned rats. In rats subjected to both hypoxic preconditioning and immobilization, the weights of the thymus, adrenal glands, and spleen, as well as cortisol level did not differ from the corresponding parameters in rats subjected to immobilization stress alone. The number of stomach ulcers in experimental rats was 1.5-fold lower than in the stress-control ones. Thus, hypoxic preconditioning exerts a pronounced preventive anti-ulcer effect during immobilization, but it does not affect other indices of the stress reaction.

[[Role of dyslipidemia in pathogenesis of vascular events among Arctic Circle population].

Habitation within the polar circle increases cardiovascular mortality rate and particularly increases mortality as a result of coronary events. The main reason of elevation of mortality from these diseases is a dyslipidemia which developed more among alien population residing long time in Far North. Dyslipidemia is less found among aboriginal population of Arctic Circle keeping traditional way of life and respectively it is low rate of mortality from coronary heart disease. The data showed that low rate of dyslipidemia among aboriginal population of North regions depends on fish consumption which is high content of Ω3-polyunsaturated fatty acids.

[Role of thyroid system in adaptation to cold].

Adaptation to cold promotes an increase in blood T3 and T4 levels in men and animals. The long-term cold exposure can induce a decrease in concentration of serum total and free T3 in human due to an enhancement of this hormone clearance. Endogenous catecholamines during adaptation to cold raise iodothyronine deiodinase D2 activity in brown fat due to α1-adrenergic receptor stimulation. Triiodothyronine is an inductor of iodothyronine deiodinase expression in brown fat, liver and kidney. Iodothyronine deiodinase D2 plays an important role in adaptation of organism to cold contributing to the high adrenergic reactivity of brown fat. At adaptation to cold T3 interacts with T3Rß, it is formed T3Rß-RXR complex, which binds to DNA with following transcription of UCP-1 and UCP-3 genes and UCP-1 and UCP-3 protein synthesis and uncoupling oxidative phosphorylation and an increase in heat production, where T3Rß is T3-receptor-ß, RXR is retinoid X-receptor, UCP is uncoupling protein. Triiodothyronine contributes to normal response to adrenergic agents of brown fat due to T3Rα activation. Sympatho-adrenomedullary and thyroid systems act as synergists in adaptation to cold.

[Influence of long-term adaptation to cold on the state of cardiovascular system].

The inhabitancy in Far North increases a probability of development of coronary heart disease, acute myocardial infarction and arterial hypertension. Catecholamines and NO deficiency play a substantial role in the development of cold hypertension, but these are not involved in acclimatization cardiac hypertrophy. Data of in vivo experiments indicate in favor of an involvement of α-adrenergic receptors (ARs) in the mechanism of an appearance of cold hypertension. Cold acclimatization promotes an elevation of ß3-AR density and decrease in ß1-AR and ß2-AR quantity on sarcolemma of cardiomyocytes. Experimental data indicate the important role of aldosterone and angiotensin II in the development of acclimatization hypertension. Catecholamines, aldosterone and angiotensin II are not involved in cold hypertrophy of heart. Experimental data demonstrate the important role of endothelin ETA receptor in the formation of cold hypertrophy of heart and cardiofibrosis. Thyroid hormones play substantial role in the development of cold hypertension and cardiac hypertrophy.