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Pharmacokinetic and pharmacodynamic factors play important roles in alcohol-drug interactions. The combined acute administration of alcohol and many other drugs may result in potentially harmful interactions especially when central nervous system depressants are involved. Often the mechanisms responsible for an adverse alcohol-drug interaction include inhibition of biotransformation and enhancement of the central depressant effects. Long-term ingestion of alcohol can lead to hepatic enzyme induction and in many instances to enhanced biotransformation of numerous substances, usually resulting in reduced therapeutic effectiveness. Alcohol-drug interactions do not generally result in death, however, there is evidence for a contributory role of alcohol in many drug-related fatalities. The elderly and chronic drug users and abusers are especially at risk.

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Two lines of rats, 'least affected' (LA) and 'most affected' (MA), had been selectively bred for their differential sensitivity to ethanol. Both males and females of the LA strain were observed to be less sensitive than their MA counterparts to the acute hypnotic and motor-impairing effects of ethanol. However, a lower ethanol metabolic rate of the MA males suggests that both CNS and metabolic factors contribute to their enhanced sensitivity to ethanol. By contrast, no differences were observed between the LA and MA males with respect to the hypnotic and subhypnotic effects of pentobarbital or to the clearance of this drug. MA females were more sensitive only to the hypnotic effects of pentobarbital, probably because of a smaller apparent volume of distribution. No strain difference was observed in the hypnotic effect or clearance of barbital. These observations suggest that, in spite of a differential sensitivity to ethanol, the LA and MA lines do not differ in their response to the barbiturates tested.

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