Abstract

Beta-phenylisopropylhydrazine (JB-516, PIH, Catron) produces a variety of pharmacological actions due to inhibition of monoamine oxidase (MAO) and because of its structural similarity to amphetamine. A comparison with some actions of another MAO inhibitor, 1-isonicotinyl-2-isopropylhydrazine (iproniazid, Marsilid) has been made.

Injection of single lethal and sublethal doses of PIH in conscious animals produced behavioral changes and signs of autonomic nervous system stimulation.

The mean arterial pressure of anesthetized dogs was raised by closes of PIH from 0.05 to 5 mg/kg. This rise in pressure was blocked by Dibenzyline but not altered by BOL-148 or TEA. PIH and amphetamine exhibited cross tachyphylaxis.

In anesthetized dogs, PIH pretreatment causes a reversal of the usual depressor response of reserpine. This "reserpine reversal" was blocked by Dibenzyhine but unaffected by BOL-148 or TEA.

PIH, in doses of from 0.25 to 5 mg/kg, produced an attenuation of the carotid sinus reflex (CSR) elicited by compression of both common carotid arteries of anesthetized dogs.

Mice injected with reserpine at various time intervals after PIH showed intense sympathetic stimulation instead of the usual sedation typical of reserpine administered alone. This effect of PIH is correlated with inhibition of brain MAO. Iproniazid was considerably less effective.

Hexobarbital sleep in mice pretreated with PIH was prolonged. Iproniazid, in a dose which produces 100% inhibition of MAO in brain and liver, was much more effective in prolonging hexobarbital sleep than a dose of PIH which yields maximum inhibition of brain and liver MAO.