1. The administration of a single oral dose of 2, 3, 4 or 5 g of ethanol/kg (43.5, 65.2, 87.0 or 108.7 mmol/kg respectively) to rats increases the rate of oxygen consumption by liver slices from animals killed 24–48 h later.

2. The increase in the rate of hepatic respiration can be blocked by incubation in a medium containing ouabain, an inhibitor of the sodium pump, or in a calcium-free medium.

3. The enhancement of oxygen uptake caused by a single dose of ethanol can be abolished by adrenalectomy or by prior administration of the α-adrenergic blocking agent phentolamine, and is markedly less in thyroidectomized animals.

4. It is suggested that the effect which is elicited by acute ethanol administration on respiration by liver slices is mediated by adrenaline and by thyroid hormones, both of which appear to exert a calorigenic effect by activation of the sodium pump. The results are discussed in relation to the changes in liver oxidative capacity induced by chronic alcohol ingestion.

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