Abstract
The present study aimed to assess the possible antinociceptive effect of cardiotonic steroids during the development of alcoholic neuropathy. The pathology was formed in rodents by means of forced alcohol consumption in increasing concentration. The force consumption of high doses of alcohol for 8 weeks allowed us to model a symptomatic complex typical for alcoholic neuropathy. During consequent modelling of the acute alcohol withdrawal syndrome, it was established that on the second day after the withdrawal there was an increase in the renal excretion of marinobufagenin, an alpha-1 isoform inhibitor of Na/K-ATPase, with a simultaneous increase in the threshold of tactile allodynia; that indicated the involvement of cardiotonic steroids in the process of nociception in alcohol dependence. The concentration of marinobufagenin in urine was measured by enzyme-linked immunoassay. It was also demonstrated that intraperitoneally administered ouabain, an alpha-3 isoform inhibitor of Na/K-ATPase, significantly increased the threshold of tactile allodynia, indicating a pronounced analgesic effect of the steroid. These data suggest that the system of Na/K-ATPase and its endogenous ligands has therapeutic potential against the development of chronic pain associated with alcohol dependence.
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