Abstract

A single large peroral dose of ethanol (3 g/kg) caused death within 12 hr after administration to rats pretreated with triiodothyronine (0.15 mg/kg/day on 6 successive days). Compared with the slight combined metabolic and respiratory acidosis observed in euthyroid controls 3 hr after ethanol administration, the triiodothyronine-pretreated rats developed only a milder acidosis of respiratory origin. Concentrations of serum Na +, Cl −, K +, Ca 2+, and Mg 2+ as well as red cell K + content were within normal limits in both hyper- and euthyroid rats 3 hr after ethanol administration. Pretreatment with 4-methylpyrazole or pyrithioxin did not affect the mortality rate or the time course of mortality after ethanol administration in the triiodothyronine-intoxicated rats. It is concluded that respiratory depression induced by ethanol does not play any significant role in the increased toxicity of ethanol in the hyperthyroid state. Nor are blood glucose or ion disturbances great enough to afford the primary cause of death. The results suggest that tissue sensitivity in the central nervous system to high ethanol concentrations per se is increased in the hyperthyroid state, but the actual mechanisms which contribute to this phenomenon are still unresolved.

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