Monoamine oxidase with barbiturates

Morphine and other opioids exhibit intense sedative effects and increased respiratory depression when combined with other sedatives, such as alcohol or barbiturates. Increased sedation and toxicity are observed when morphine is administered in combination with the psychotropic drugs, such as chlorpromazine and monoamine oxidase inhibitors, or the anxiolytics, such as diazepam. 

Chlorazepate potentiates the CNS-depressant effects of phenothiazines, narcotics, barbiturates, alcohol, antihistamines, monoamine oxidase inhibitors, general anesthetics, and antidepressants. Concomitant use with cimetidine and possibly disulfiram causes diminished hepatic metabolism of chlorazepate, which increases its plasma concentration. 

Some of the monoamine oxidase inhibitors prolong the hexobarbitone sleeping time in mice, probably because they inhibit barbiturate breakdown by the liver microsomes . An anticonvulsive action has also been reported . The fact that the hydrazine derivatives interact with pyridoxal phosphate and can thus inhibit GABA formation may explain why some of the inhibitors of this type sometimes have a convulsive action also. 

Drug Interactions Barbiturates combine with other CNS depressants to cause severe depression ethanol is the most frequent offender, and interactions with first-generation antihistamines also are common. Isoniazid, methylphenidate, and monoamine oxidase inhibitors also increase the CNS-depressant effects. Other prominent drag interactions occin as a result of the induction of hepatic drug-metabolizing enzymes by barbiturates see above). 

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