Analysis of changes in the serotonin inactivation coefficient in brain structures with simultaneous modeling of chronic neurogenic pain and malignant neoplasia

Introduction . Chronic pain syndrome in the development of malignant neoplasms has a complex polyethological character. The study pathogenetic mechanisms during growth transplanted tumor experiment can open up broad perspectives for creation new domestic analgesic drugs use oncology. Aim : To serotonin inactivation coefficient (SIC), ratio (S) and its main metabolite 5-hydroxyindolacetic acid (S-OH) brain areas (cortex, hypothalamus) with simultaneous modeling chronic neurogenic neoplasia. Material Methods involved white mongrel rats (males). create model (CP), ligation sciatic nerve was performed according to method V.V. Kravtsova modification. Rat sarcoma M-1 used simulate At stage study, animals were divided into 4 groups: control, two comparison groups (model pain, standard grafting) experimental (combined CP oncological process). Animals second, third fourth euthanized sequentially at 2nd 3rd weeks process. Results disrupts process metabolism: decrease SIC cerebral cortex more significant by 48% (day 14) 72% 21). (groups 3a 3b) is accompanied level SIC, 21th day development: 37% hypothalamus, 41% cortex. With neoplasia, lowest values studied indicator noted, 75% (group 4a) 87% 4b). Discussion isolated variants cause hypothalamus due disorders formation. A disruption mediator system noted which leads body’s adaptive capabilities regulatory metabolism. Conclusion Modification metabolism be considered as potential therapeutic target treatment