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PubMed1998

Effect of desipramine on immunological parameters in mice, and their reversal by stress.

Immunomodulation of cell-mediated immunity is demonstrated in mice, after administration of desipramine, a noradrenaline-reuptake inhibitor, with or without exposing the mice later to an acute swimming stress. A single i.p. injection of 10 mg/kg desipramine to naive mice increased the relative weight of their spleens, the response of their splenocytes to the mitogen concavaline-A and their ability to produce IL-10, as compared to saline controls. Exposing the desipramine-treated mice to a swimming stress significantly reduced these parameters, as well as the levels of IL-2 and IFN-gamma, as compared to desipramine-treated mice. Stress alone reduced the weight of the spleen, and the ability of splenocytes to produce IFN-gamma. As desipramine and acute stress have stimulatory effect on the sympathetic system, it is suggested that a concomitant administration of the drug and a stressful event of these mice, change the splenocytes' micro-environment of sympathetic transmitters, and inhibit their function. These results may be partially due to impairment in the T-helper cell function by a beta-adrenoreceptor-dependent mechanism.

Animals↗

PubMed1996

No interaction between desipramine and bromperidol.

1. The authors studied the effects of coadministration of desipramine, which is a substrate of CYP2D6, on plasma concentrations of bromperidol and its reduced metabolite (reduced bromperidol). Clinical changes were also evaluated by the CGI and UKU. 2. The subjects were 13 schizophrenic inpatients receiving bromperidol 12.24 mg/day for 1.20 weeks. Desipramine 50 mg/day was coadministered for 1 week, and blood samplings and clinical ratings were performed before and after the coadministration. 3. Plasma concentrations of bromperidol and reduced bromperidol were measured by a HPLC method. 4. Desipramine coadministration did not affect plasma concentration of bromperidol (9.6 +/- 4.5 vs. 9.6 +/- 2.8 ng/ml) nor that of reduced bromperidol (2.8 +/- 2.5 vs. 2.8 +/- 2.1 ng/ml). 5. There was no significant change in the CGI scores nor UKU scores after desipramine coadministration. 6. The present study thus suggests that there is no interaction between desipramine and bromperidol.

Adult↗

PubMed1989

A double-blind comparison of clomipramine and desipramine in the treatment of trichotillomania (hair pulling)

Trichotillomania, an irresistible impulse to pull out one's own hair, is a chronic psychiatric illness that causes severe discomfort, interferes with daily activities, and leads to social isolation. Treatment is usually unsatisfactory. Thirteen women with severe trichotillomania completed a 10-week double-blind, crossover trial of clomipramine, a new tricyclic antidepressant agent with selective antiobsessional effects, and desipramine, a standard tricyclic antidepressant. Treatment with clomipramine resulted in significantly greater improvement in symptoms than desipramine, as indicated by physicians' ratings of the women's clinical progress on a scale in which lower scores indicate improvement (mean [+/- SD] scores: at base line, 10.0; after desipramine treatment, 8.7 +/- 2.4; after clomipramine treatment, 4.7 +/- 3.1; P = 0.006) and by scores on a trichotillomania-impairment scale, in which higher scores indicate greater impairment (at base line, 6.8 +/- 1.7; after desipramine treatment, 6.2 +/- 1.7; after clomipramine treatment, 4.2 +/- 2.7; P = 0.03). The severity of symptoms (mean base-line score, 15.9 +/- 3.8) was reduced more by clomipramine (10.6 +/- 6.4) than by desipramine (14.4 +/- 3.9). The patients reported that the compulsion decreased in intensity and that they were more able to resist the urge to pull out their hair during treatment with clomipramine. We conclude that clomipramine appears to be effective in the short-term treatment of trichotillomania.

Adolescent↗

PubMed1993

Enhancement by the tricyclic antidepressant, desipramine, of experimental carcinogenesis in rat colon induced by azoxymethane.

The effects of the tricyclic antidepressant drug desipramine on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the serum norepinephrine (NE) concentration and the labeling index of colon mucosa were investigated in Wistar rats. Rats were treated s.c. with 7.4 mg AOM/kg body wt once a week for 10 weeks, and also s.c. with 10 mg desipramine hydrochloride (desipramine)/kg body weight until the end of the experiment. Treatment with desipramine significantly increased the incidence, but not the number, of colon tumors in week 35. However, it did not influence the location and the histological appearance of the colon tumors or the histological types of colon adenocarcinomas. Furthermore, it significantly increased the serum NE level and the labeling index of colon mucosa during and after AOM treatment. These findings indicate that desipramine enhanced the development of colon tumors and that its effect may be related to its effect in increasing proliferation of colon epithelial cells.

Animals↗

PubMed1996

Rauwolscine potentiates the effect of desipramine on limbic noradrenaline efflux.

Desipramine, like most antidepressants, does not exert clinical benefit until 2-3 weeks after the onset of treatment. It has been suggested that this delay might be due to enhanced autoreceptor activation, counteracting the acute uptake blockade. We therefore tested whether autoreceptor blockade might enhance the response to acute uptake blockade, using voltammetry at carbon fibre microelectrodes to monitor stimulated noradrenaline (NA) efflux in rat bed nucleus of stria terminalis brain slices. Desipramine significantly increased NA efflux and slowed NA uptake. The combination of rauwolscine and desipramine increased NA efflux significantly more than desipramine alone. We suggest that alpha 2 autoreceptor blockade functionally mimics alpha 2 autoreceptor down-regulation and thus may allow the full therapeutic effect of desipramine to be manifested more rapidly.

Adrenergic Uptake Inhibitors↗

PubMed1989

Cardiovascular effects of desipramine in children.

The effect of desipramine hydrochloride was studied in children who were treated for eating disorders (5), attention deficit disorder (13), or affective disturbance (3). Serial heart rate, blood pressure, ECG, and 24-hour ambulatory monitoring were recorded before treatment and at 4 and 8 weeks during treatment. Maximum dose of desipramine was 5 mg/kg/day, average 4.25. A 21% increase in heart rate and 2.5% increase in QTc at 4 weeks were sustained at 8 weeks. No dysrhythmias or clinically significant changes in blood pressure occurred. Desipramine is safe in children who have normal cardiovascular examinations and ECGs when used within the limits of the study design. The cardiovascular effects of desipramine should be kept in mind and monitored when patients are starting tricyclic antidepressant therapy such as desipramine.

Arrhythmias, Cardiac↗

PubMed2000

Therapeutic effects of imipramine are counteracted by its metabolite, desipramine, in patients with generalized anxiety disorder.

Imipramine has been shown to reduce anxiety in patients with generalized anxiety disorder (GAD). However, some properties of imipramine may diminish or counteract its anxiolytic effects. The authors previously found that the greater the reduction in cardiac vagal control after 6 weeks of imipramine treatment, the smaller the improvement in anxiety-related symptoms. The purpose of this study was to determine whether the authors' previous findings were replicable and to gather information on the plasma levels of imipramine, desipramine (the major metabolite of imipramine), and anticholinergic levels. Fourteen patients with GAD were administered imipramine for 6 weeks. Their scores from self-administered and investigator-administered rating scales were obtained before and after the treatment, and the changes in these scores were contrasted with the changes in cardiac vagal tone, along with the absolute plasma levels of imipramine, desipramine, and anticholinergic activity at the end of week 6. The authors observed a greater improvement in symptoms of anxiety in those who showed the smallest decreases in cardiac vagal tone and in those who showed the smallest increases in desipramine and anticholinergic plasma levels. Moreover, strong relationships were observed between desipramine and anticholinergic levels. These results demonstrate that imipramine not only has therapeutic effects, but it may also have properties that result in physiologic states that counteract its therapeutic effects. Future research should investigate the direct anticholinergic effects of desipramine and determine whether there is a parallel between the anticholinergic effects and the clinical outcome of other pharmacologic treatments, including antidepressants with predominantly norepinephrine or serotonin reuptake inhibitory properties.

Adrenergic Uptake Inhibitors↗

PubMed1985

Comparison of the effects of chronic administration of ciclazindol and desipramine on pupillary responses to tyramine, methoxamine and pilocarpine in healthy volunteers.

Twenty-nine healthy volunteers participated in an experiment lasting for 8 weeks: Phase I (2 weeks)--pre-treatment control period; Phase II (4 weeks)--medication with either ciclazindol hydrochloride (50 mg twice daily), or desipramine hydrochloride (50 mg twice daily) or lactose placebo (twice daily) administered in a single-blind fashion; Phase II (2 weeks)--recovery. Experimental sessions took place twice weekly for the photographic assessment of resting pupil diameter, and for the assessment of one of the following pupillary responses: mydriatic response to methoxamine, mydriatic response to tyramine, miotic response to pilocarpine. Resting pupil diameter increased during medication with either ciclazindol or desipramine. Methoxamine-evoked mydriasis and tyramine-evoked mydriasis were antagonized by both ciclazindol and desipramine. Pilocarpine-evoked miosis was potentiated by both ciclazindol and desipramine. The steady-state plasma levels (mean +/- s.e. mean) of the antidepressants were: ciclazindol: 5.90 +/- 0.74 microM; desipramine: 0.60 +/- 0.17 microM. The antagonism of methoxamine-evoked mydriasis is likely to reflect the blockade of postsynaptic alpha 1-adrenoceptors in the iris by the antidepressants, whereas the antagonism of tyramine-evoked mydriasis may reflect both the blockade of uptake of tyramine into presynaptic adrenergic terminals and the blockade of postsynaptic alpha-adrenoceptors. There is no immediate explanation for the potentiation of pilocarpine-evoked miosis by the two antidepressants.

Adolescent↗

PubMed1990

Effect of desipramine on a glycoprotein sialyltransferase activity in C6 cultured glioma cells.

The tricyclic antidepressant desipramine, when added to culture medium, gave rise in C6 rat glioma cells to a decrease of the activity of the enzyme asialofetuin sialyltransferase. The inhibition was dose and time dependent and was observed in both multiplying cells and cells blocked with 2 mM thymidine or depletion of amino acids. This inhibition was rather specific to the sialyltransferase, as under the conditions where this enzyme was inhibited up to 70%, other enzymes such as dolichol phosphate mannose synthetase, glutamine synthetase, and glycerol phosphate dehydrogenase remained unaffected. This inhibition was not reversed after removal of desipramine from the medium and was not observed by direct addition of desipramine to the sialyltransferase incubation assay. Under the same conditions, W-7 [N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide], which is known to be a potent calmodulin antagonist and an inhibitor of calmodulin-dependent kinases, gave the same concentration-dependent inhibition profile of sialyltransferase as desipramine, whereas H-7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine], which is an inhibitor of protein kinase C and cyclic nucleotide-dependent kinases, had no effect. So, it is suggested that desipramine inhibits the sialyltransferase activity in C6 glioma cells through a calmodulin-dependent system.

Animals↗

PubMed1981

Effects of mianserin, desipramine and maprotiline on blood pressure responses evoked by acetylcholine, histamine and 5-hydroxytryptamine in rats.

1 In rats anaesthetized with pentobarbitone, intravenous administration of desipramine (0.1 mg/kg), maprotiline (0.5 mg/kg) or mianserin (0.3-3.0 mg/kg) did not modify the blood pressure lowering effects of acetylcholine (0.25-1.0 micrograms/kg, i.v.) which were significantly reduced by atropine (3.0 micrograms/kg, i.v.). 2 Maprotiline and mianserin, like promethazine (0.1 mg/kg, i.v.), inhibited the vasodepressor responses evoked by histamine (2.5-10.0 micrograms/kg,i.v.). however, desipramine was inactive against histamine. 3 In pithed rats, the pressor effects of intravenous 5-hydroxytryptamine (5-HT: 5.0-20.0 micrograms/kg) were antagonized by mianserin (0.01-0.3 mg/kg, i.v.) and cyproheptadine (0.01 mg/kg) but were unaffected by maprotiline and desipramine. 4 In syrosingopine pretreated rats given mianserin 0.1 mg/kg, intravenously, 5-HT (20.0 micrograms/kg, i.v.) produced a significant fall in blood pressure which could be reduced by a large dose of mianserin (10.0 mg/kg, i.v.). 5 In conclusion, desipramine, maptrotiline and mianserin, in doses previously found to inhibit noradrenaline neuronal reuptake in the rat cardiovascular system, lack muscarinic receptor antagonist properties. Whilst maprotiline and mianserin blocked vascular histamine receptors, only mianserin (10.0 mg/kg, i.v.). 5 In conclusion, desipramine, maptrotiline and mianserin, in doses previously found to inhibit noradrenaline neuronal reuptake in the rat cardiovascular system, lack muscarinic receptor antagonist properties. Whilst maprotiline and mianserin blocked vascular histamine receptors, only mianserin, like cyproheptadine, was a potent antagonist of the 5-HT receptors that mediate increases in blood pressure in rats. Finally, the vasodepressor effects of 5-HT in syrosingopine pretreated rats given a small dose of mianserin were antagonized by a large dose of mianserin, suggesting that 5-HT may activate two distinct types of receptors in the rat.

Acetylcholine↗

PubMed1991

Determination of the role of noradrenergic and 5-hydroxytryptaminergic neurones in postsynaptic alpha 2-adrenoceptor desensitization by desipramine and ECS.

1. Experiments were conducted to determine the respective roles which noradrenergic and 5-hydroxytryptaminergic neurones play in the down-regulation of postsynaptic alpha 2-adrenoceptors by desipramine and electroconvulsive shock (ECS). The functional status of these receptors was monitored by use of clonidine-induced mydriasis in conscious mice. 2. Mydriasis to clonidine (0.1 mg kg-1, i.p.) was markedly attenuated by administration of either desipramine (10 mg kg-1, i.p.) for 14 days or ECS (200 V, 2s) given five times over ten days confirming our previous observations. 3. The neurotoxin, DSP-4 (100 mg kg-1, i.p. X 2), reduced brain noradrenaline levels by 64% and abolished the mydriasis induced by the noradrenaline releasing agent and reuptake inhibitor, methamphetamine, without significantly altering the response to clonidine, confirming our earlier results. This lesion prevented the attenuation of clonidine mydriasis by repeated administration of desipramine, but not ECS. 4. Lesioning of central 5-hydroxytryptaminergic neurones with 5,7-dihydroxytryptamine (75 micrograms, i.c.v.) had no influence on the reduction in clonidine mydriasis produced by repeated administration of either desipramine or ECS. 5. Since noradrenergic neurones are essential for the desensitization of postsynaptic alpha 2-adrenoceptors by desipramine, it indicates that this effect is probably the result of increased synaptic noradrenaline levels. This mechanism is not responsible for the change induced by ECS because this adaptation is independent of an intact noradrenergic input. 5-HT-containing neurones do not play a permissive role in the down-regulation of postsynaptic alpha 2-adrenoceptors by either antidepressant treatment.

Animals↗

PubMed1990

Moclobemide (Ro 11-1163) versus desipramine in the treatment of endogenous depression.

Moclobemide was compared with desipramine in 30 patients with endogenous depression. The Hamilton Rating Scale for Depression showed significantly greater improvement for moclobemide (69%) than for desipramine (45%). The final assessment of tolerance was good or very good in 87% of moclobemide patients compared with 13% of desipramine patients; 5 patients in the first group and all 15 in the second group complained of adverse effects. One patient on moclobemide and 5 on desipramine stopped treatment prematurely because of poor tolerance; no patients stopped treatment because of lack of efficacy. Assessment in this study was made difficult by concomitant treatment with benzodiazepines and/or mild neuroleptics in both groups, but the results of efficacy and tolerance clearly favour moclobemide over desipramine in the treatment of endogenous depression in hospitalized patients.

Antidepressive Agents↗

PubMed1992

Different desipramine-sensitive pulmonary removals of plasma epinephrine and norepinephrine in dogs.

The lungs are an important site for the clearance of norepinephrine from the circulation, but the mechanism of removal and its importance for clearance of epinephrine require clarification. In the present study, 3H-labeled epinephrine and norepinephrine were infused intravenously into anesthetized dogs, and blood samples were taken from the pulmonary artery and aorta to compare pulmonary extractions of both catecholamines before and after administration of the neuronal uptake blocking drug, desipramine. Circulating [3H]norepinephrine and [3H]-epinephrine were both extracted by the lungs, but fractional extraction of [3H]epinephrine (8.1 +/- 1.1%) was half that of [3H]norepinephrine (16.9 +/- 1.9%). Pulmonary extractions of both catecholamines were completely blocked by desipramine. Desipramine-sensitive removal accounted for a tenth of the total body extraction of [3H]epinephrine and a third that of [3H]norepinephrine. Pulmonary removal of [3H]epinephrine was 14% that of the total body clearance, whereas pulmonary removal of [3H]norepinephrine was 25% that of the total body clearance. The study showed the following: removal of catecholamines by the canine lung in vivo is by desipramine-sensitive uptake; uptake is half as efficient for epinephrine as norepinephrine: and, pulmonary removal contributes importantly to the desipramine-sensitive component of total body catecholamine clearance.

Animals↗

PubMed1990

Successful treatment of nonpurging bulimia nervosa with desipramine: a double-blind, placebo-controlled study.

Twenty-three women with nonpurging bulimia underwent a 12-week, double-blind, placebo-controlled trial of desipramine hydrochloride. Repeated standardized rating scales, mood assessments, and self-reports of dietary habits were used to measure changes in binge frequency and cognitive processes associated with food intake. The women who received desipramine reduced their frequency of binge eating by 63%, but women receiving placebo increased their frequency of binge eating by 16%. Twelve weeks after initiating treatment, 60% of the treatment group but only 15% of the placebo group abstained from binge eating. The women who received desipramine showed significantly more dietary restraint and reported significantly less hunger, suggesting that desipramine acts to suppress appetite. These preliminary findings suggest that the therapeutic effects of desipramine established in the treatment of purging bulimia nervosa extend to patients with nonpurging bulimia.

Appetite↗

PubMed1992

Differential response of seven subjects with autistic disorder to clomipramine and desipramine.

OBJECTIVE: Clomipramine, a serotonin reuptake blocker that has unique antiobsessional properties, was hypothesized to have a different effect from that of desipramine, a tricyclic antidepressant with selective adrenergic effects, for the stereotyped, repetitive behaviors in autism. METHOD: Seven subjects, ages 6-18 years, with autistic disorder completed a 10-week double-blind, crossover trial of clomipramine and desipramine following a 2-week single-blind, placebo phase. RESULTS: Clomipramine was superior to desipramine and placebo, as indicated by standardized ratings of autism and anger as well as ratings of repetitive and compulsive behaviors. Clomipramine and desipramine were equally superior to placebo for ratings of hyperactivity. Parents of all seven subjects elected to have their children continue to take clomipramine after the study. CONCLUSIONS: Clomipramine and desipramine are differentially effective in treating the obsessive-compulsive and core symptoms in autistic disorder. Biological links between compulsions and stereotyped, repetitive behaviors in autistic disorder should be explored.

Adolescent↗

PubMed2002

Effect of terbinafine on the pharmacokinetics and pharmacodynamics of desipramine in healthy volunteers identified as cytochrome P450 2D6 (CYP2D6) extensive metabolizers.

Terbinafine-CYP2D6 inhibition was evaluated by assessing 48-hour concentration-time profiles of the tricyclic antidepressant desipramine in 12 healthy volunteers identified as extensive cytochrome P450 2D6 (CYP2D6) metabolizers by genotyping and phenotyping. Pharmacokinetics was evaluated at baseline (50 mg oral desipramine given alone), steady state (after 250 mg oral terbinafine for 21 days), and 2 and 4 weeks after terbinafine discontinuation. Pharmacodynamics was evaluated before and 2 hours after each desipramine administration, using Mini-Mental Status Examination (MMSE) and EGG. Terbinafine administration inhibited CYP2D6 metabolism, as indicated by the significant increase in desipramine C(max) (19 ng/ml vs. 36 ng/ml) and AUC0-infinity (482 ng.h/ml vs. 2383 ng.h/ml) and decrease in AUC0-24 and C(max) of the CYP2D6-mediated metabolite, 2-hydroxydesipramine. In addition, the C(max) and AGUC0-infinity of desipramine and metabolite were still elevated 4 weeks after terbinafine discontinuation. Caution should be exercised when coprescribing terbinafine and drugs metabolized by CYP2D6, particularly those with a narrow therapeutic index.

Adolescent↗

PubMed1988

Treatment of bulimia with desipramine: a double-blind crossover study.

The purpose of this study was to evaluate the effect of desipramine, a tricyclic antidepressant with relatively specific noradrenergic effects, on bulimic behaviour, eating attitudes, and mood. Using a double-blind crossover design, 47 normal weight bulimics were randomly assigned to receive either desipramine (150 mg/day) for six weeks, no drug for three weeks, followed by placebo for six weeks, or the reverse sequence. At weeks 0, 2, 4, 6, 9, 11, 13, and 15, each subject was assessed using the EDI, SCL-90, POMS and binge records. Plasma desipramine levels were obtained at weeks 4 and 13. Twenty-four subjects completed the entire fifteen week protocol, while 23 dropped out. Desipramine was significantly more effective than placebo in reducing the frequency of weekly binding, weekly vomiting, and the fatigue scale of the POMS. No significant effect of the drug was obtained on the EDI or the SCL-90. The clinical effect was modest. Desipramine's antibulimic effects were not associated with an alleviation of depressive symptoms.

Adult↗

PubMed1987

Desipramine-, not tartrazine-, induced drug eruption.

A 46-year-old woman's antidepressant therapy was changed from doxepin to desipramine because of sedative side effects. Within ten days of initiation of desipramine, a pruritic, morbilliform rash developed. The rash extended despite attempts to continue therapy with a tartrazine-free desipramine as well as antihistamines and prednisone. The rash promptly improved when desipramine was discontinued. Classic drug eruptions are quite uncommon with tricyclic antidepressants. Tartrazine, a common additive in the food and drug industry, is implicated in a number of hypersensitivity reactions. Our report presents an apparent case of desipramine-induced drug rash independent of tartrazine, and discusses the nonassociation of tartrazine.

Azo Compounds↗