ABSTRACT
The development of delayed disorders caused by acute ethylene glycol poisoning has been studied in experiments on male rats. These disorders include chronic renal failure and secondary combined immunodeficiency status of the "circulus vitiosus" type. Urgent pharmacological correction was shown to be necessary shortly after the poisoning. The experimental therapy (administration of immunomodulators with various mechanisms of action in addition to conventional antidote treatment with ethanol) resulted in the restoration of nonspecific resistance and both cellular and humoral immunity. Reduction of the urinary system damage after the administration of immunomodulators was observed. The results demonstrated the importance of multiagent immunotherapy for the correction of delayed effects of acute ethylene glycol poisoning.
Subject(s)
Acridines/pharmacology , Dipeptides/pharmacology , Immunologic Deficiency Syndromes/prevention & control , Immunologic Factors/pharmacology , Kidney Failure, Chronic/prevention & control , Animals , Antidotes/pharmacology , Blood Glucose/analysis , Creatinine/blood , Cytokines/blood , Ethanol/pharmacology , Ethylene Glycol , Immunity, Humoral/drug effects , Immunity, Innate/drug effects , Immunologic Deficiency Syndromes/chemically induced , Immunologic Deficiency Syndromes/complications , Kidney Failure, Chronic/chemically induced , Kidney Failure, Chronic/complications , Kidney Function Tests , Lactic Acid/blood , Male , Rats , Rats, Wistar , Sodium Bicarbonate/pharmacologyABSTRACT
The effect of remaxol therapy as a part of the complex acute treatment of ethylene glycol poisoning has been experimentally studied on rats. Special attention was paid to the development of acidosis and hypoxia and a decrease in the functional activity of the urinary and immune systems. It was shown that remaxol is capable of restoring the functional activity of organs and systems susceptible to the toxic effect of ethylene glycol. It is suggested that the therapeutic efficiency of remaxol is based on the normalization of metabolic processes in the cell.
