Induction of phencyclidine metabolism by phencyclidine, ketamine, ethanol, phenobarbital and isosafrole.

The in vitro metabolism of phencyclidine (PCP) was investigated in 9000 g supernatant fractions of both control and PCP-, ketamine-, ethanol-, phenobarbital- or isosafrole-pretreated rats. Levels of PCP, trans-4-phenyl-4-piperidinocyclohexanol (I), 1-(1-phenylcyclohexyl)-4-hydroxypiperidine (II), N-(5-hydroxypentyl)-1-phenylcyclohexylamine (IX), and 5-(1-phenylcyclohexylamino)-valeric acid (X) were monitored by gas chromatographic analysis in all cases. The inhibition of metabolism by N2, CO, SKF-525A or 2,4-dichloro-6-phenylphenoxyethylamine (DPEA), or deletion of NADPH or protein, implied the involvement of cytochrome P-450 in the reactions.

Morphine suppression of bradycardia induced by electrical stimulation of gigantocellular reticular nucleus in the cat.

In chloralose-urethane-anesthetized cats, intravertebral injection of morphine (1,2 and 4 mg/kg) promoted a drastic suppression of the bradycardia elicited by stimulating the medullary gigantocelular reticular nucleus (GRN). The degree of blockadge of GRN-induced cardioinhibition was directly dependent upon the dose of morphine and inversely related to the reticular stimulus train intensity and pulse frequency. The possibility that the GRM may be a site of action for morphine in its production of hypotension and bradycardia was discussed.