Release of thyroidal serotonin by reserpine, methyldopa and guanethidine

Magus, Raymond D.; Krause, Fred W.; Riedel, Bernard E.

doi:10.1016/0006-2952(64)90085-1

Cited by 7 publications

(1 citation statement)

References 9 publications

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“…of ice-cold 0.01 N hydrochloric acid. The monoamines were extracted simultaneously from the homogenates using the method of Magnus, Krause & Riedel (1964). Aliquots of the final acid extract were used for the assay of noradrenaline (Shore & Olin, 1958), dopamine (Costa, Gessa, Kuntzman & Brodie, 1962) and 5-hydroxytryptamine (Bogdanski, Pletscher, Brodie & Udenfriend, 1956).…”

Section: Methodsmentioning

confidence: 99%

The interaction between monoamine oxidase inhibitors and narcotic analgesics in mice

Rogers

Thornton

1969

British J Pharmacology

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1. The administration of either iproniazid or tranylcypromine to mice potentiates the acute toxicity of pethidine, morphine, pentazocine and phenazocine. 2. Blood levels of pentazocine in mice pretreated with tranylcypromine do not differ from the levels in animals not receiving the monoamine oxidase (MAO) inhibitor. 3. There is no correlation ibetween changes in brain and liver MAO activity and the increased pethidine toxicity. 4. A comparison is made between the change in pethidine toxicity and the changes in the concentration of cerebral noradrenaline, dopamine and 5-hydroxytryptamine following the injection of tranylcypromine. 5. It is concluded that the increased toxicity of potent analgesics in combination with MAO inhibitors is not due to a decelerated meta(bolism of the analgesic drug, but is related to an increases concentration of cerebral 5-hydroxytryptamine. A critical level of this monoamine, in the brain, may be necessary before the drug interaction will take place.Monoamine oxidase (MAO) inhibitors are known to potentiate the effects of a wide variety of pharmacological agents, and severe toxic reactions have been observed when certain drugs have been given to patients receiving MAO inhilbitors for the treatment of depressive states. This group of drug interactions has been the subject of reviews (by Goldiberg (1964) and Sjoquist (1965). The majority of the .adverse reactions are caused by agents which, like MAO inhilbitors, exert an effect on monoaminergic neurotransmission. Some drugs, however, interact with MAO inhibitors by mechanisms which remain to be fully elucidated. The narcotic analgesics, and in particular pethidine, provide an example.The adverse reaction to pethidine is said to be due to a decelerated breakdown 'of the analgesic drug, since MAO inhibitors are known to exert non-specific effects on detoxifying enzyme systems in the liver. A decelerated breakdown of pethidine would explain an exaggeration of the normal response to this drug, namely hypotension and respiratory depression, but it does not explain other reported effects such as hypertension and hyperpyrexia, effects which occur soon after the administration of pethidine to patients receiving MAO inhilbitors (Rogers, Jepson, Kilpatrick & Thornton, unpublished). Furthermore, although the toxicity of other potent

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Section: Methodsmentioning

confidence: 99%