Relevance. It is known that in traumatic brain injury (TBI), the activity of the central cholinergic systems (CChS) is inhibited, the release of acetylcholine and the expression of cholinergic receptors decrease. The restoration of cholinoreactivity is an urgent area of research and a possible therapeutic direction.
Objective – to determine the effect of CChS activation on mortality, neurological disorders, and the activity of the pituitary-corticoadrenal system (PCAS) in the acute period of TBI.
Material and methods. TBI was simulated with a free load’s fall on a fixed animal head. To activate the CChS, rats were injected with choline alfoscerate (gliatilin, 6 mg/kg) before the injury, physiological saline was injected in the control group. Neurological deficits were assessed using the 100-point Todd scale. In blood plasma, 3, 24, 48, and 72 hours after injury, the content of adrenocorticotropic hormone and corticosterone was determined by the enzyme immunoassay method (DSL; USA). The results were statistically processed using the SPSS 11.0, MedStat, MedCalc software.
Results. Mortality in the control group was 25.0%, in the group with activation of the CChS there were no lethal cases (p<0.05). The neurological deficit in the group with CChS activation was significantly less pronounced compared to the control at all periods of observation. The hormone content had a similar dynamics: it reached a maximum after 24 hours and recovered after 72 hours, however, upon activation of the CChS, the increase was 1.4-1.5 times less (p<0.05). Thus, the use of choline alfoscerate for modeling the CChS activity led to a decrease in mortality and neurological deficit in the acute period of TBI, which was accompanied by a stabilizing PCAS function.
Conclusion. The important role of CChS in the implementation of post-traumatic stress reaction of PCAS, as well as the possibility of its pharmacological correction with choline alfoscerate, was established.
Possibilities of applying ethylmethylhydroxypyridine succinate in comprehensive intensive therapy of acute period of traumatic brain injury
