ВНУТРИ- И МЕЖСИСТЕМНЫЕ МЕХАНИЗМЫ РЕГУЛЯЦИИ ГОМЕОСТАЗА КАЛИЯ В ОНТОГЕНЕЗЕ
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statistically insignificant. This parameter tended to decrease in passive rats (by 9.1%), but increased in active animals (by 34.4% compared to the baseline). Passive specimens demonstrated an insignificant decrease in TFL on day 1 after the induction of stroke (by 7.2% compared to the baseline). By contrast, this parameter was revealed to increase by 26.1% in active rats (p<0.05). No significant changes were found in VT of animals. On day 3 of the post-stroke period, all rats were characterized by the following changes in TFL (p<0.05 compared to the baseline): decrease by 13.6% in passive specimens, and increase by 35.2% in active animals. During this stage of observations the level of VT remained practically unchanged in passive rats, but slightly increased in active specimens (by 19.7%). On day 7 after modeling of stroke, statistically significant changes in TFL were observed only in active animals (45.0% increase compared to the baseline, p<0.05). By contrast, this parameter tended to decrease by 13.1% in passive rats. Variations in VT during this period were similar in behaviorally passive and active specimens (increase by 11.7 and 37.7%, respectively, compared to the baseline). Hence, behaviorally passive and active rats with stress-induced hemorrhagic stroke are characterized by opposite changes only in the perceptual component of nociception. The observed increase in nociceptive sensitivity of passive specimens is consistent with the results of clinical observations, which illustrate the development of post-stroke pain syndrome . We revealed that the perceptual component of nociception in behaviorally active animals is diminished during the post-stroke period. It is a new fact in studying the consequences of stress-induced hemorrhagic stroke. These data illustrate the specifics of changes in pain sensitivity of specimens with different stress resistance at various stages of the post-stroke period. REFERENCES 1. A. Yu. Abramova, S. S. Pertsov, A. Yu. Kozlov, et al., Byull. Eksp. Biol. Med., 155, No. 4, 404-409 (2013). 2. N. O. Ivannikova, S. S. Pertsov, and V. V. Krylin, Byull. Eksp. Biol. Med., 153, No. 5, 653-658 (2012). 3. A. Yu. Kozlov, A. Yu. Abramova, V. V. Chekhlov, et al., Byull. Eksp. Biol. Med., 159, No. 6, 676-680 (2015). 4. E. V. Koplik, Vestn. Nov. Med. Tekhnol., 9, No. 1, 16-18 (2002). 5. R. A. Harrison and T. S. Field, Cerebrovasc Dis., 39, No. 3 4, 190-201 (2015). DOI:10.12737/12277 ВНУТРИ- И МЕЖСИСТЕМНЫЕ МЕХАНИЗМЫ РЕГУЛЯЦИИ ГОМЕОСТАЗА КАЛИЯ В ОНТОГЕНЕЗЕ Р.И.Айзман ФГБОУ ВПО «Новосибирский государственный педагогический университет» (ректор – А.Д.Герасёв) firstname.lastname@example.org