Pharmacological correction of neurotoxic damage in severe acute ethanol poisoning

Abstract

Alcohol abuse currently poses a serious health problem in many countries worldwide. High levels of alcohol consumption in Russia are responsible for the large number of acute alcohol and alcohol-additive poisonings recorded in recent decades. Particularly significant is the shift in the pattern of alcohol poisoning, with a predominance among middle-aged and young adults, as well as an increase in the incidence of such poisoning in children. Along with significant mortality due to the inability to provide timely medical care, a serious consequence of acute severe alcohol poisoning is dysfunction of various tissues and organs, manifesting in the late, somatogenic stage of intoxication. Among these, neurotoxic damage is noteworthy. Ethanol is classified as a neurotoxicant, i.e., a substance whose toxic effect involves damage to various structural elements of the nervous system, primarily the central nervous system. Neurotoxic damage, a consequence of severe acute alcohol poisoning that significantly impacts the social status and quality of life of this patient group, including leading to disability, has been insufficiently studied. The aim of this study was to investigate the nature and severity of neurotoxic damage in rats following severe acute ethanol poisoning and to substantiate the possibility of pharmacological correction of the identified disorders. Using a battery of tests, we comprehensively assessed behavior, motor activity, motor coordination, muscle strength, cognitive functions, and pain perception in rats that had suffered severe acute ethanol poisoning. The use of neuroprotective agents---picamilon, a derivative of nicotinic and γ-aminobutyric acid, and noopept, a dipeptide drug, and their combination---for the correction of neurotoxic damage in the somatogenic stage of acute ethanol poisoning is justified.