SEARCH · PubMed Health

Results for “DESIPRAMINE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources

PubMed1984

Double-blind comparison of desipramine and placebo in withdrawal from cocaine dependence.

Desipramine was compared with a placebo under double-blind conditions to determine if it is effective treatment for withdrawal from cocaine dependence. Eleven (11) subjects received desipramine and 11 received placebo. There was no significant statistical difference between groups in self-report on effectiveness; retention in treatment; cessation of cocaine use; or suppression of withdrawal scores. Although desipramine appears to be no more effective than placebo in withdrawal from cocaine use or suppression of withdrawal scores, it may be useful in the long-term treatment of this condition.

Adolescent↗

PubMed1982

ECG effects of comparable plasma concentrations of desipramine and amitriptyline.

To compare the electrocardiographic effects of therapeutic doses of desipramine and amitriptyline, weekly electrocardiograms (ECGs) were obtained from 46 depressed outpatients treated blindly for 3 weeks to a maximum of 200 mg/day. There was no difference in mean weekly plasma tricyclic antidepressant levels achieved for the two drugs. Compared to baseline measures, treatment with both drugs was associated with an increase in heart rate and a reduction in T wave amplitude, whereas prolongation of the QRS and QTc intervals was significant only for desipramine patients. Comparisons between drugs revealed a greater prolongation of QRS interval duration with desipramine treatment. Changes in ECG measures were not correlated with plasma tricyclic antidepressant levels. The absence of QRS interval prolongation among amitriptyline patients is additional evidence for the importance of distinguishing between the ECG effects of therapeutic and toxic doses of the tricyclic antidepressant.

Adult↗

PubMedDate not supplied

Minaprine, but not oxiracetam, prevents desipramine-induced impairment of avoidance learning in mice.

The tricyclic antidepressant desipramine impaired shuttle-box avoidance acquisition in mice of the CD-1 strain. The nootropic drug oxiracetam was unable to prevent the desipramine-induced learning impairment, while a protective action was exerted by minaprine, a psychotropic agent regarded as an atypical antidepressant drug, possessing dopaminergic and related memory-enhancing properties. It seems likely that the dopaminergic action of minaprine played a determinant role in its avoidance improving effects in desipramine treated mice, because similar effects were produced by amphetamine. However, in contrast to amphetamine, minaprine did not enhance locomotor activity and did not show signs of general behavioral stimulation.

Animals↗

PubMed1995

A double-blind comparison of clomipramine and desipramine in the treatment of developmental stuttering.

BACKGROUND: Clomipramine, a serotonin reuptake blocker that has been shown to be effective in treating obsessive-compulsive disorder and other unwanted repetitive, ritualized behaviors, was hypothesized to be superior to desipramine, a tricyclic antidepressant with selective noradrenergic effects, for developmental stuttering. METHOD: Seventeen psychiatrically normal subjects, aged 14-61 years, with developmental stuttering completed a 10-week double-blind crossover trial of clomipramine and desipramine after a 2-week single-blind placebo phase. RESULTS: Clomipramine was superior to desipramine (two-tailed, p < .05) for 5 of 10 self-report ratings including stuttering severity on two scales, degree of preoccupation with stuttering and resistance to stuttering on a visual analog scale, and "expectancy" of stuttering on the Perceptions of Stuttering Inventory. CONCLUSION: Clomipramine may be clinically useful for some patients with developmental stuttering. Biological links between developmental stuttering and other repetitive motor patterns that are selectively responsive to serotonergic agents should be explored.

Adolescent↗

PubMedDate not supplied

[Psychotropic profile of essential antidepressants (amitriptyline, imipramine, desipramine, chlorimipramine): comparative study].

Comparative studies of the therapeutic activity of amitriptyline, imipramine, desipramine and chlorimipramine were studied in a group of 185 patients with endogenous depression. After standard 28-day treatment, the best results were obtained while using amitriptyline (improvement rate 67%, the greatest reduction in the Hamilton Depression Scale scored on 28-day of the treatment). The profile and characteristics of antidepressive action of all the drugs taken into consideration are comparable (including slightly more expressed sedative and deliberative effects of amitriptyline). Desinhibitive influence of desipramine and imipramine was not proved. Neither was tachythymoleptic activity of desipramine found. The study does not support the relation between the antidepressive action profile of tricyclic antidepressants and their influence on reuptake of monoamines (norepinephrine and serotonine).

Adult↗

PubMed1997

Paradoxical action of desipramine on the modulatory effect of bradykinin on noradrenaline release in a model of metabolic anoxia in rat isolated atria.

We have previously shown that bradykinin (BK) can modulate the release of noradrenaline (NA) in a model of metabolic anoxia in the rat isolated atria. In this study, we tested the effect of an inhibitor of NA reuptake, desipramine, on the modulatory action of BK on NA release in this experimental model. Atria were isolated from Wistar rats and inserted into a perfusion system. After an equilibration period of 20 min, the perfusate was collected every 5 min for a period of 85 min, during which the atria were field stimulated (5 Hz, 2 ms, 50 mA, 60 s) at 10 (S1) and 75 (S2) min. Desipramine (1 microM) was present throughout the experimental procedures. The metabolic anoxia was started 40 min before S2 by replacing O2 with N2 and by removing glucose. The drugs were added 20 min before S2, and their effects were assessed by the ratio S2/S1. The spontaneous release of NA was not changed by the anoxic procedure, which significantly increased the electrically stimulated induced (S-I) release of NA. BK (30 nM) significantly increased the S-I release of norepinephrine under normoxic conditions. However, following anoxia, both BK and the B1 receptor agonist des-Arg9-BK (100 nM) significantly inhibited the S-I release of NA. The inhibition induced by BK was prevented by selective antagonists for B1 and B2 receptors. These observations contrast with the results obtained without desipramine, where BK, but not des-Arg(9)-BK, inhibited the S-I release of NA during anoxia. Therefore, blockade of NA reuptake during metabolic anoxia appears to alter the modulatory effect of kinins on NA release via the B1 receptor in the rat isolated atria.

Adrenergic Uptake Inhibitors↗

PubMed1998

Effects of electroconvulsive therapy and desipramine on neuroendocrine responses to the clonidine challenge test.

OBJECTIVE: To investigate responses to the clonidine challenge test in depression, and after electroconvulsive therapy (ECT) or desipramine treatment for depression, in order to determine the usefulness of noradrenergic responses to clonidine as a state or trait marker in depression. PATIENTS: Twenty-six patients with depression and 15 control subjects. SETTING: The psychiatric ward of St. Joseph's Hospital in Hamilton. INTERVENTIONS: In the patients with depression: clonidine challenge pre- and post-treatment with ECT or desipramine. In the controls: 2 clonidine challenge tests 4 to 8 weeks apart. OUTCOME MEASURES: The primary measure was the growth hormone response to the clonidine challenge. Plasma norepinephrine, 3-methoxy-4-hydroxyphenylglycol (MHPG), cortisol, blood pressure, pulse and sedation levels were examined in subgroups of participants as secondary measures. RESULTS: The pre-treatment growth hormone response to clonidine was significantly more blunted in patients than in controls (p = 0.02). This response improved in both treatment groups after therapy and, although it remained decreased, there was no longer a significant difference in response between the patients and the controls. In the patients, a decreased growth hormone response to clonidine at baseline was correlated with response to treatment. Of the secondary measures, patient baseline norepinephrine levels were significantly elevated pre- and post-treatment, although there were no significant group-by-time challenge effects. MHPG levels were not significantly different pre- and post-treatment between patients and controls. Baseline blood pressure and pulse were elevated in the patients pre- and post-treatment. These differences were not statistically significant and did not change after treatment. Sedation levels were not significantly different among the groups at baseline. Clonidine-induced sedation occurred significantly earlier in the patients pretreatment and improved to the range of the controls after treatment. Pretreatment cortisol response was significantly more blunted in the patients who received ECT than in the controls; however, the group-by-time effect post-treatment was no longer significant. DISCUSSION: Treatment with either desipramine or ECT modified noradrenergic functioning in patients with depression, as assessed by growth hormone response to the clonidine challenge. In the patients, a decreased growth hormone response at baseline was correlated with clinical response. Changes between pre- and post-treatment measures suggest that this challenge test may not be sensitive enough to serve as a trait marker but may correlate with the state of depression in a subpopulation of these patients.

Adrenergic alpha-Agonists↗

PubMed1993

Another sudden death in a child treated with desipramine.

The sudden death of three children receiving the tricyclic antidepressant medication desipramine for behavioral disorders was reported in 1990. We now provide new information about these children and describe a fourth case. Because desipramine is a useful medication for many children, these deaths pose clinical dilemmas for physicians and families. The cardiac long QT syndrome has been proposed as a mechanism for these sudden deaths. Considerable uncertainty remains about the basis of the apparent association between the use of desipramine and the sudden deaths.

Attention Deficit Disorder with Hyperactivity↗

PubMed1980

Single-dose kinetics predict steady-state concentrations on imipramine and desipramine.

Single-dose prediction of ultimate steady-state concentrations of tricyclic antidepressants at the outset of treatment can be a valuable therapeutic tool that has had only limited application. We demonstrate accurate steady-state predictions following both the tertiary amine, imipramine hydrochloride, and the secondary amine, desipramine hydrochloride, in a carefully monitored long-term treatment patient population. Results show that long-term treatment does not alter metabolism of either imipramine or desipramine. The relative merits of single-dose predictions using total and "abbreviated" areas under the curve and concentration at 24 hours are compared. These findings demonstrate that single-dose prediction can be used as a practical therapeutic, as well as, research tool.

Adolescent↗

PubMed1984

Cocaine abuse treatment. Open pilot trial with desipramine and lithium carbonate.

We conducted an open clinical trial of desipramine hydrochloride or lithium carbonate as adjuncts to psychotherapy in cocaine abusers. Subjects who were treated with desipramine hydrochloride showed marked decreases in a measure of cocaine craving after two to three weeks of treatment and became abstinent regardless of whether an affective disorder was also present. Lithium carbonate was effective only in cyclothymic subjects. Other subjects treated with lithium carbonate, as well as nonpharmacologically treated subjects, continued their cocaine use.

Adult↗

PubMed1986

Treating bulimia with desipramine. A double-blind, placebo-controlled study.

A controlled study in patients with bulimia demonstrated a significant benefit from desipramine hydrochloride treatment (91% decrease in binge frequency) in contrast to the results from a placebo (19% increase in frequency). When patients originally taking the placebo crossed over to desipramine therapy, their frequency of binges decreased 84%, so that the overall improvement was 87% fewer binges. Global clinical status improved 3.5 scales, Zung depression scores improved 8.0 points, and a bulimia symptom scale improved 14.7 points. Fifteen (68%) of 22 patients attained complete abstinence from binge eating and purging. The presence or absence of previous episodes of anorexia nervosa did not influence the treatment response. One-month follow-up data indicated persistence of the benefit attained.

Adolescent↗

PubMed1989

Effects of desipramine and fluvoxamine treatment on the prolactin response to tryptophan. Serotonergic function and the mechanism of antidepressant action.

It has been hypothesized that enhancement of brain serotoninergic (5-HT) function is involved in the mechanism of action of some antidepressants. To test this, the prolactin response to intravenously administered tryptophan, a clinical measurement of 5-HT function, was assessed before and during antidepressant treatment. Depressed patients received the tricyclic desipramine hydrochloride (N = 24) or the 5-HT reuptake inhibitor fluvoxamine maleate (N = 30). The prolactin response was significantly enhanced after long-term treatment (4 weeks) but not as reliably increased after short-term (1-week) desipramine treatment. Fluvoxamine enhanced the prolactin response after both short- and long-term treatment. Enhancement of the prolactin response was not clearly correlated with clinical improvement. The results of this study are consistent with preclinical evidence of enhanced 5-HT function during treatment with these classes of antidepressants, but also indicate that enhanced 5-HT function is not a sufficient condition for antidepressant efficacy.

Antidepressive Agents↗

PubMed1991

Desipramine lowers tritiated para-aminoclonidine binding in platelets of depressed patients.

Platelet adrenergic receptor binding has been studied by several groups of investigators as a possible marker for depression and other psychiatric conditions. Although some of the findings have been discrepant, the results of the majority of studies that have used imidazoline compounds as ligands have confirmed elevated alpha 2-adrenergic receptor binding in depression. We have emphasized the advantages of obtaining platelet-purified plasma membranes and using tritiated para-aminoclonidine as the ligand of choice. By using "site-selective" concentrations of tritiated para-aminoclonidine, we have identified two high-affinity-binding sites of the platelet alpha 2-adrenergic receptor that appear to be upregulated in depression before treatment. Depressed patients were treated with desipramine hydrochloride for 6 to 8 weeks, and platelet binding was reassessed. Desipramine reduced binding to nearly normal levels at both site-selective concentrations of tritiated para-aminoclonidine. The concentrations of plasma catecholamines could play a role in the downregulation of binding at posttreatment. We discuss these findings in the context of platelet imidazoline-binding sites being a possible state-dependent marker for depression.

Adrenergic alpha-Agonists↗

PubMed1991

A double-blind comparison of clomipramine and desipramine treatment of severe onychophagia (nail biting).

Twenty-five adult subjects with severe morbid onychophagia (nail biting) and no history of obsessive-compulsive disorder were enrolled in a 10-week double-blind cross-over trial of clomipramine hydrochloride and desipramine hydrochloride. For the 14 subjects who completed the study, clomipramine hydrochloride (mean +/- SD dose, 120 +/- 48 mg/d) was superior to desipramine hydrochloride (mean +/- SD dose, 135 +/- 53 mg/d) in decreasing nail biting as measured by a repeated-measures analysis of variance on the Nail Biting Severity, Nailbiting Impairment, and Clinical Progress scales. The high dropout rate at every stage of the study was in sharp contrast to that seen with psychiatric populations. From a neuroethologic perspective, similar biologic systems are hypothesized to mediate a spectrum of grooming behaviors, including onychophagia, trichotillomania, and obsessive-compulsive disorder.

Adult↗

PubMed1991

A double-blind desipramine substitution during long-term clomipramine treatment in children and adolescents with obsessive-compulsive disorder.

Twenty-six children and adolescents with severe primary obsessive-compulsive disorder receiving long-term clomipramine hydrochloride maintenance treatment (mean +/- SD, 17.1 +/- 8.3 months; range, 4 to 32 months) entered an 8-month double-blind desipramine hydrochloride substitution study to assess the necessity of continued drug treatment. All patients received clomipramine for the first 3 months, then half continued with clomipramine therapy (nonsubstituted group) and half had desipramine blindly substituted for the next 2 months; all subjects again received clomipramine for the last 3 study months. Eight (89%) of nine of the substituted and only two (18%) of 11 of the nonsubstituted group subjects relapsed during the 2-month comparison period. Long-term clomipramine treatment seems necessary for this population of children and adolescents with obsessive-compulsive disorder. However, even patients receiving maintenance clomipramine treatment throughout the entire study had continued obsessive-compulsive symptoms, which varied in severity over time.

Adolescent↗

PubMed1992

Pharmacotherapy for cocaine-abusing methadone-maintained patients using amantadine or desipramine.

In a double-blind, placebo-controlled 12-week randomized clinical trial, we compared amantadine hydrochloride (300 mg/d; n = 33), desipramine hydrochloride (150 mg/d; n = 30), and placebo (n = 31) in the treatment of cocaine-abusing methadone-maintained patients. Treatment retention and medication compliance were excellent, with more than 75% of the patients completing the full 12-week trial. Although reported cocaine abuse was significantly lower in the medicated groups compared with the placebo group at week 4, this difference became nonsignificant at week 8, and no difference was found in cocaine-free urine samples. Future studies of amantadine and desipramine treatment in these patients should consider alternatives to methadone hydrochloride, such as buprenorphine hydrochloride, and the selection of more homogeneous patient subgroups, such as depressed cocaine abusers.

Adult↗

PubMed1998

Adolescent depression: controlled desipramine treatment and atypical features.

The study was designed to test the efficacy of desipramine in adolescents with major depression (MDD). In addition, we assessed the presence of atypical features of MDD, consisting of mood reactivity and two of four associated features (rejection sensitivity, hyperphagia, hypersomnia, and leaden paralysis). Patients were randomized to desipramine (DMI) or placebo for 6 weeks, provided they failed to improve (e.g., meeting MDD criteria and a Hamilton Depression Scale score > or = 18) after 2 weeks on single blind placebo. Of 94 adolescents (ages 13-18) who were diagnosed as having MDD, 64 entered the study and 62 received placebo for 2 weeks. Of these, 45 were randomized to DMI or placebo. Completed analyses did not reveal significant improvement for the active treatment compared to the placebo. A large proportion of adolescents responded to placebo (50%), suggesting the need for very large samples to detect differential treatment efficacy, should it exist. A relatively high rate of atypical depression was observed (47% in the 64 patients entered). In view of the demonstrated specificity of monoamine oxidase inhibitor efficacy in adults with atypical features of MDD, this clinical subtype may have relevance to future investigation of therapeutic interventions in adolescent MDD.

Adolescent↗

PubMed2005

Therapeutic monitoring of imipramine and desipramine by micellar liquid chromatography with direct injection and electrochemical detection.

A micellar liquid chromatographic (MLC) procedure was developed for the clinical monitoring of imipramine and its active metabolite, desipramine. The determination of these highly hydrophobic substances was carried out after direct injection of the serum samples using a mobile phase composed of 0.15 m SDS--6% (v/v) pentanol buffered at pH 7, pumped at 1.5 mL/min into a C(18) column (250 x 4.6 mm), and electrochemical detection at 650 mV. Using this MLC method, calibration was linear (r > 0.995) and the limits of detection (ng/mL) were 0.34 and 0.24 for imipramine and desipramine, respectively. Repeatabilities and intermediate precision were tested at three different concentrations in the calibration range and a CV (%) below 2.2 was obtained. In this MLC procedure, the serum is determined without treatment, thus allowing repeated serial injections without changes in retention factors, and reducing the time and consumables required to carry out the pretreatment process. The assay method can be applied to the routine determination of serum imipramine and its metabolite in therapeutic drug monitoring.

Antidepressive Agents, Tricyclic↗