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Eur Neuropsychopharmacol ; 25(11): 2183-4, 2015 Nov.
Article in English | MEDLINE | ID: mdl-26302763

ABSTRACT

Ketamine, a rapid-acting antidepressant and anti-suicidal agent, is thought to increase brain monoamine levels by enhancing monoamine release or inhibiting presynaptic monoamine-reuptake. Here we present two female inpatients suffering from treatment-resistant depression with recurrent severe suicidal crises receiving a combination of intravenous S-ketamine and oral tranylcypromine, which is a well-known irreversible monoamine oxidase (MAO) inhibitor. Since inhibition of monoamine-reuptake with concurrent blockade of MAO might trigger sympathomimetic crisis, this combination is considered hazardous. Nonetheless, cardiovascular parameters remained stable in both patients, while good anti-suicidal effects were observed. Hence, we put serious doubt on whether monoamine-reuptake inhibition is a relevant pharmacological effect of ketamine in humans.


Subject(s)
Antidepressive Agents/administration & dosage , Depressive Disorder, Treatment-Resistant/drug therapy , Ketamine/administration & dosage , Tranylcypromine/administration & dosage , Administration, Intravenous , Administration, Oral , Adult , Aged , Female , Humans , Inpatients , Monoamine Oxidase Inhibitors/administration & dosage , Suicide Prevention
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