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PubMed1983

Effects of amitriptyline, desipramine and mianserin on noradrenergic transmission in the rat isolated right ventricle.

The effects of amitriptyline, desipramine and mianserin on the accumulation of radioactivity from [3H]-noradrenaline, and on the subsequent spontaneous and field stimulation-evoked outflow of radioactivity have been investigated in the rat isolated right ventricle. In addition the effect of these agents on contractions produced by isoprenaline or by field stimulation are reported. Amitriptyline, desipramine (both at greater than or equal to 10(-8) M) and mianserin at greater than or equal to 10(-7) M inhibited the accumulation of radioactivity from [3H]-noradrenaline. The decline in the spontaneous outflow of radioactivity, following loading of the tissue with [3H]-noradrenaline, was not altered by amitriptyline, desipramine or mianserin. Rauwolscine, amitriptyline, desipramine and mianserin (all at 10(-6) M) reduced or reversed the decline in outflow of radioactivity evoked by field stimulation at 5 Hz. Desipramine had no additional effects in the presence of cocaine (10(-5) M) and amitriptyline and mianserin had no further effect in the presence of cocaine and rauwolscine. The effect of desipramine probably represents inhibition of neuronal uptake and that of amitriptyline and mianserin blockade of neuronal uptake and prejunctional alpha 2-adrenoreceptors. The rate of beating in the presence of isoprenaline (10(-6) M) was reduced by amitriptyline (10(-7) M), desipramine (10(-6) M) and mianserin (10(-7)--10(-6) M). Higher concentrations of the antidepressants greatly reduced or abolished the rate and force of beating in the presence of isoprenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Amitriptyline↗

PubMed1972

Uptake of desipramine by the rat vas deferens.

1. Determinations of desipramine in the isolated rat vas deferens were carried out in order to study the uptake of the drug and to evaluate how this may correlate with the effect on noradrenaline (NA)-induced contraction.2. Vasa deferentia, in contact with concentrations of desipramine of 1 ng-25 mug/ml for 10 min accumulated the drug about 6-fold in respect to the medium. When the time of contact was prolonged to 4 h, desipramine (200 ng/ml) was concentrated about 100-fold. The uptake was not saturable and it was not affected by the presence of imipramine, cocaine, ouabain, dinitrophenol and iodoacetate.3. No metabolic process is involved although the accumulation of desipramine is temperature dependent. The release of desipramine from the vas deferens is exponential and it is not affected by the presence of plasma in the medium.4. No clear correlation was found between tissue concentration of the drug and the potentiation of noradrenaline responses, probably because of the high non-specific binding of the drug to tissue components which may mask specific binding sites for NA resulting in potentiation. However, the concentration of desipramine seems to correlate with the inhibition of NA effect which occurs at high doses of desipramine.

Animals↗

PubMed1977

Plasma concentrations and cardiotoxic effects of desipramine and protriptyline in the rat.

1 Desipramine and protriptyline were administered to anaesthetized rats by two consecutive intravenous infusions in order to obtain a peak level (first infusion) followed by lower steady state concentrations (second infusion) (Wagner, 1974). Theoretical plasma level time courses were confirmed experimentally.2 Desipramine and protriptyline were measured in atria and ventricles. Increasing infusion rates led to proportional increases in plasma and atrial concentrations. The tissue/medium ratio ranged from 57 to 21 for desipramine and from 43 to 11 for protriptyline according to the time of determination during infusions.3 Heart rate changes, deviation of the electrical axis of the heart and prolongation of atrioventricular conduction were recorded at fixed times during infusion.4 Positive chronotropic effects were noted at plasma concentrations ranging from 0.035 to 0.1 mug/ml for desipramine and from 0.04 to 1.2 mug/ml for protriptyline. At higher plasma concentrations the positive chronotropic effect decreased and bradycardia developed. Both drugs induced right rotation of the electrical axis of the heart. Threshold plasma levels giving 40 degrees rotation were 1.35 mug/ml (desipramine) and 1.75 mug/ml (protriptyline). Atrioventricular conduction was prolonged at threshold plasma concentrations of 2.2 mug/ml for desipramine and 3.6 mug/ml for protriptyline.5 Desipramine is more cardiotoxic than protriptyline. This difference is discussed in relation to the plasma and heart concentration of the two drugs.

Animals↗

PubMed2003

Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion.

We reported recently that inhibition of neuronal reuptake of norepinephrine (NE) by desipramine prevented the reduction of sympathetic neurotransmitters in the failing right ventricle of right heart failure animals. In this study, we studied whether desipramine also reduced the sympathetic neurotransmitter loss in animals with left heart failure induced by rapid ventricular pacing (225 beats/min) or after chronic NE infusion (0.5 microg. kg(-1). min(-1)). Desipramine was given to the animals for 8 wk beginning with rapid ventricular pacing or NE infusion. Animals receiving no desipramine were studied as controls. We measured myocardial NE content, NE uptake activity, and sympathetic NE, tyrosine hydroxylase, and neuropeptide Y profiles by histofluorescence and immunocytochemical techniques. Effects of desipramine on NE uptake inhibition were evidenced by potentiation of the pressor response to exogenous NE and reduction of myocardial NE uptake activity. Desipramine treatment had no effect in sham or saline control animals but attenuated the reduction of sympathetic neurotransmitter profiles in the left ventricles of animals with rapid cardiac pacing and NE infusion. In contrast, the panneuronal marker protein gene product 9.5 profile was not affected by either rapid pacing or NE infusion, nor was it changed by desipramine treatment in the heart failure animals. The study confirms that excess NE contributes to the reduction of cardiac sympathetic neurotransmitters in heart failure. In addition, it shows that the anatomic integrity of the sympathetic nerves is relatively intact and that the neuronal damaging effect of NE involves the uptake of NE or its metabolites into the sympathetic nerves.

Adrenergic Fibers↗

PubMed1995

Retreatment for relapse following desipramine discontinuation in dysthymia.

OBJECTIVE: It is an accepted yet unproven belief that prior favorable response to an antidepressant medication predicts good response to the same antidepressant during a subsequent depressive episode. The authors studied desipramine retreatment for dysthymic patients who had responded to desipramine during acute and continuation treatment and then subsequently relapsed after discontinuation of desipramine. METHOD: The subjects were 12 patients who had pure dysthymia or dysthymia with major depression who relapsed while taking placebo during maintenance treatment. Each patient received open desipramine treatment at a dose equal to or greater than that received during the continuation phase. RESULTS: Eleven (91.7%) of the 12 relapsed patients achieved full remission after an average of 4.7 weeks (range = 2-8 weeks, median = 4 weeks) of desipramine retreatment, a significant response rate. CONCLUSIONS: Positive response to desipramine strongly predicts favorable response to retreatment for depressive relapse following desipramine discontinuation.

Adult↗

PubMed1996

Six-week, double-blind, placebo-controlled study of desipramine for adult attention deficit hyperactivity disorder.

OBJECTIVE: Despite the increasing awareness of attention deficit hyperactivity disorder (ADHD) in adults, there are a limited number of controlled pharmacologic studies of this disorder; most of the trials have focused on the psychostimulants. Because the tricyclic anti-depressant desipramine has been found to be effective in treating ADHD in pediatric groups, the authors tested its efficacy in adults with ADHD. METHOD: The authors conducted a randomized, 6-week, placebo-controlled, parallel-design study of desipramine at a target daily dose of 200 mg in 41 adult patients with DSM-III-R ADHD. They used standardized structured psychiatric instruments for diagnosis and, as the dependent variables (outcome), used separate assessments of ADHD, depressive, and anxiety symptoms at baseline and at each biweekly visit. RESULTS: There were highly significant differences in the reduction of ADHD symptoms between adults receiving desipramine and placebo. Within the desipramine-treated group, there were clinically and statistically significant differences between baseline and the week 6 end point for 1) reduction of 12 of 14 symptoms of ADHD and 2) decreases in the broad categories of hyperactivity, impulsivity, and inattentiveness. In contrast, placebo-treated patients showed no differences between baseline and end point for any of the ADHD symptoms assessed. According to strict, predefined criteria for response, 68% of desipramine-treated subjects and no subjects in the placebo group were considered positive responders. Response to desipramine was independent of dose, level of impairment, gender, or lifetime psychiatric comorbidity with anxiety or depressive disorders. CONCLUSIONS: These results, similar to findings in children and adolescents with ADHD, indicate that desipramine is effective in the treatment of ADHD in adults.

Adolescent↗

PubMed1990

Clinical pharmacokinetics of imipramine and desipramine.

The pharmacokinetics of imipramine and desipramine have been extensively investigated with recent studies designed to understand sources of intersubject variability and to study discrete clinical populations rather than healthy volunteers. Sources of intersubject variability in pharmacokinetics are both genetic (oxidative phenotype) and environmental. Oxidative phenotype has an important impact on first-pass metabolism. In individuals with poor metabolism, systemic availability for imipramine is increased. Intrinsic clearance of desipramine is reduced 4-fold in individuals with poor metabolism. Recent pharmacokinetic studies in diverse patient populations such as the depressed elderly, children and alcoholics have revealed decreased clearance of imipramine in the elderly and increased clearance of both imipramine and desipramine in chronic alcoholics. In at least a third of the population, nonlinear pharmacokinetics of desipramine may be observed at steady-state plasma concentrations above 150 micrograms/L. These nonlinear changes in desipramine pharmacokinetics are not associated with age or sex, but are associated with higher desipramine 2-hydroxydesipramine concentration ratios. Hydroxylated metabolites of imipramine and desipramine may possess both antidepressants and cardiotoxic activity but their formation is rate limited and plasma concentrations tend to follow the parent compound with little accumulation. The potent cardiovascular effects of the hydroxymetabolites may be particularly relevant for the elderly and in acute overdose.

Biological Availability↗

PubMed1976

Relationships between chronotropic effect, 1-3H-noradrenaline uptake and tissue concentrations of desipramine, protripyline and doxepin in rat isolated atria.

The pharmacological effects of three tricyclic antidepressant agents (desipramine, protriptyline and doxepin) are evaluated in rat isolated atria in relation to their accumulation and efflux kinetics. The pharmacological effects studed are: inhibition of 1-3H-noradrenaline uptake, potentiation of 1-noradrenaline chronotropic response, and changes in spontaneous atrial rate. All drugs inhibit noradrenaline uptake and potentiate noradrenaline chronotropic response (desipramine congruent to protriptyline greater than doxepin). Desipramine and protriptyline, at concentrations of 10(-7) -- 10(-6)M stimulate the spontaneous rate; higher concentrations (greater than 10(-6)M) depress it. Doxepin has only a negative chronotropic effect. When the drugs are removed from the incubation medium, the depressing effect starts to disappear immediately for doxepin and desipramine and after 20 min for protriptyline. On the contrary the stimulating effect persists after repeatedly washing the preparations. Desipramine, protriptyline and doxepin extensively accumulate in the myocardial tissue (desipramine larger than or equal to protriptyline greater than doxepin). In the efflux studies doxepin is washed out more rapidly than desipramine and protriptyline. Although the kinetics of uptake and efflux of the three compounds are not sufficient to interpret their different pharmacological activities in isolated atria, they give useful information on the persistance of the sympathomimetic effect and the rapid disappearing of the negative chronotropic effect after washing.

Animals↗

PubMedDate not supplied

Effect of repeated desipramine and fluoxetine administration on post-adjuvant arthritis.

The effects of desipramine and fluoxetine on the swelling of hind paws, radiologically-detectable bone destruction of hind paws, increase in spleen and popliteal lymph node weight, increase in metabolic activity of splenocytes and increase in proliferative activity of splenocytes and popliteal lymph node cells from right adjuvant injected paw in male C57BL/6 mice were studied on the 17th day after induction of post-adjuvant arthritis. Drugs were administered once-daily ip at a dose of 10 mg/kg. Fourteen days of desipramine administration, starting on the third day after injection of the adjuvant, significantly increased edema and radiologically assessed bone destruction, spleen and popliteal lymph node weight whereas fluoxetine induced an opposite effect, but it did not reduce edema in comparison with saline-treated control. Two-week desipramine administration significantly increased metabolic activity of splenocytes and proliferative activity of popliteal lymph node cells from the right adjuvant-injected paw, whereas 14 days of fluoxetine injection reduced proliferative activity of splenocytes in comparison with the saline-treated mice. Desipramine administration 30 days before and 17 days after adjuvant injection did not change these parameters in spite of reduction of proliferative activity of splenocytes. These findings indicate that: 1) fluoxetine has a suppressive effect on some of the local and systemic changes which occur in adjuvant-induced arthritis in mice, 2) two-week desipramine administration significantly increases whereas 47-day desipramine treatment does not change most of local and systemic parameters of post-adjuvant disease in C57BL/6 mice, 3) the action of fluoxetine differs from that of desipramine in this model of autoimmunodisease probably as a result of the distinct effect of these two drugs on corticoids levels and on the activity of a sympathetic nervous system.

Animals↗

PubMed1989

Determination of serum desipramine and 2-hydroxydesipramine for pharmacokinetic applications by HPLC with ultraviolet detection.

This procedure for measuring desipramine and its 2-hydroxy metabolite in serum at a minimum concentration of 1 micrograms/L involves high-performance liquid chromatography (HPLC), with ultraviolet detection at 214 nm. After desipramine and 2-hydroxydesipramine are extracted from alkalinized serum by a single-step solvent extraction, they are separated by HPLC and quantified with amitriptyline as the internal standard. Desipramine, 2-hydroxydesipramine, and amitriptyline are separated in 6 min. The standard curve is linear (r = 1.000) for both desipramine and 2-hydroxydesipramine concentrations over the range of 1 to 100 micrograms/L, and the assay demonstrates an excellent precision profile, even at low concentrations. Between-run CVs for 20 and 60 micrograms/L controls (n = 20) were 3.9% and 3.6% for desipramine and 3.4% and 3.8% for 2-hydroxydesipramine, respectively. In a pharmacokinetic evaluation of patients with depression, we examined single-dose elimination curves before and after a four-week regimen of desipramine treatment. The results showed that the method's simplicity and high precision render it ideal for pharmacokinetic studies of desipramine.

Alkalies↗

PubMed1985

Desipramine plasma levels and response in elderly melancholic patients.

The relationship of response and plasma desipramine concentrations was examined in elderly depressed patients to determine whether they were more sensitive to the antidepressant effects of the drug and whether they would respond at lower plasma concentrations than younger patients. Twenty-five inpatients over the age of 60, who met criteria for major depression with melancholia, were unipolar, were not delusional, were without active medical illness or definite brain disease, and were still depressed after 1 week of hospitalization off psychotropic drugs, were treated with desipramine (2.5 mg/kg) for 3 weeks. Of the 18 patients completing the drug trial, six responded and 12 did not. Desipramine levels of responders (median, 126 ng/ml) were higher than those of nonresponders (median, 81 ng/ml; Mann-Whitney test, p less than 0.05). The threshold for response was the same as the threshold (115 ng/ml) observed in 31 nondelusional melancholic patients under the age of 60 treated in a similar manner with desipramine. Among elderly patients with levels above 115 ng/ml, four of five responded, and below this level, two of 13 responded (Fisher's exact test, p less than 0.025). Five patients not responding to the initial 3-week trial responded when desipramine was increased and the plasma level rose above 115 ng/ml. The data indicate that elderly melancholic patients to not respond to lower desipramine plasma concentrations and that therapeutic levels are similar to those for younger melancholic patients. The doses of desipramine needed to reach these levels were also similar to those required in younger patients.

Adult↗

PubMed1984

Altered effects of desipramine on operant performance after 6-hydroxydopamine-induced depletion of brain dopamine or norepinephrine.

Performance maintained by differential-reinforcement-of-low-rate operant schedules has been found to be sensitive to antidepressant drugs. Tricyclic antidepressants, monoamine oxidase inhibitors and atypical antidepressants reduce response rate and increase reinforcement rate under long differential-reinforcement-of-low-rate schedules. In order to study the neurochemical mechanism by which the tricyclic antidepressant desipramine alters differential-reinforcement-of-low-rate performance, the effect of desipramine was determined before and after brain catecholamine depletion was induced by 6-hydroxydopamine administration. Before lesioning, desipramine reduced response rate and increased reinforcement rate in a dose-dependent manner. Brain norepinephrine depletion (produced by 6-hydroxydopamine injection into the dorsal noradrenergic bundle) attenuated the ability of desipramine to reduce response rate, but did not alter its ability to increase reinforcement rate, but did not alter its ability to increase reinforcement rate. Brain dopamine depletion, (produced by i.c.v. 6-hydroxydopamine administration after pargyline and desipramine pretreatment) attenuated the ability of desipramine to increase reinforcement rate. These results suggest that the sedative effect of desipramine could be mediated by its interaction with central norepinephrine neurons and that the reinforcement rate-increasing effect may involve central dopamine neurons.

Animals↗

PubMed1983

Urinary MHPG excretion and treatment with desipramine or amitriptyline: prediction of response, effect of treatment, and methodological hazards.

Urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) excretion was measured in 49 unipolar depressed outpatients to examine the relationship between pretreatment MHPG levels and therapeutic response to desipramine and amitriptyline and to determine the effects of these agents on MHPG excretion. Pretreatment MHPG excretion was greater in amitriptyline responders than amitriptyline nonresponders, but no different in desipramine responders compared to desipramine nonresponders. Pretreatment MHPG excretion did not differentiate desipramine from amitriptyline responders. Treatment for 3 weeks was associated with a decrement in MHPG excretion, particularly in the desipramine responders and combined desipramine and amitriptyline responders. Among patients within the postulated optimal desipramine plasma level range and patients with plasma amitriptyline plus nortriptyline levels greater than 70 ng/ml, high pretreatment MHPG excretion predicted therapeutic response and response was accompanied by a reduction in MHPG excretion. The interpretation of these findings is possibly confounded by the demonstration of a poor correlation (r = 0.61) between duplicate MHPG samples analyzed by a widely employed gas chromatography method and a gas chromatography/mass spectrometry technique. The methodological pitfalls encountered in the course of this investigation and their possible implications for similar studies are discussed.

Adult↗

PubMed1996

Sertraline versus desipramine in the treatment of premenstrual syndrome: an open-label trial.

BACKGROUND: Antidepressant medications have appeared to be effective treatments for premenstrual syndrome (PMS) in several small trials. This open-label study examined the efficacy of and tolerance for a new serotonergic antidepressant compared with a traditional tricyclic antidepressant in PMS treatment. METHOD: For two menstrual cycles in women meeting well-defined criteria for PMS, an open-label comparison of the serotonin selective sertraline (N = 17) and the noradrenergic desipramine (N = 15) was performed. Dose was flexible, with a mean dose in the second cycle of 87 mg/day for sertraline and 110 mg/day for desipramine. Outcome measures were the premenstrual daily symptom report (DSR) scores and the Hamilton Rating Scale for Depression (HAM-D). RESULTS: Sertraline and desipramine reduced depressive symptoms as assessed by the HAM-D, both achieving similar reductions in the HAM-D scores. Reduction of total premenstrual symptoms as assessed by the DSR score was observably greater with sertraline, but the difference compared with desipramine was not statistically significant in this small sample. Subjects were more likely to perceive desipramine side effects as intolerable; 4 of the 15 desipramine-treated subjects discontinued compared with none in the sertraline group. Subjects who were previously treated in a PMS program without good therapeutic response were less likely to respond to either medication, suggesting a treatment-resistant group. CONCLUSION: Sertraline and possibly desipramine appear to be effective treatments for PMS. Sertraline was better tolerated, resulting in greater patient acceptance. A placebo-controlled trial in which subjects are randomly assigned to the medication is clearly needed to support or refute these preliminary findings.

1-Naphthylamine↗

PubMed1996

A double-blind, placebo-controlled trial of desipramine for primary alcohol dependence stratified on the presence or absence of major depression.

OBJECTIVE: To assess the use of desipramine for secondary depression in primary alcohol dependence and its effect on abstinence. DESIGN: Randomized, double-blind, placebo-controlled trial, with stratification on the presence of secondary depression. SUBJECTS: Seventy-one volunteer and referred patients with primary alcohol dependence, abstinent a median of 8 days before randomization. A subset of 28 patients had major depression secondary to alcoholism. SETTING: The outpatient psychiatry departments of two urban medical centers. INTERVENTION: Six months of a clinically determined dose of desipramine. MAIN OUTCOME MEASURES: Hamilton Depression Rating Scale, and Time Line Follow Back Interview, with breath alcohol concentrations and collateral verification. RESULTS: Hamilton Depression scores of desipramine-treated depressed alcoholics decreased significantly, controlling for baseline Hamilton Depression scores (P=.04). Overall, patients were abstinent significantly longer when receiving desipramine (P=.03). Rates of relapse of depressed vs nondepressed patients, analyzed separately, were not significant, although the survival function approached significance for the depressed subgroup (P=.09). Desipramine-treated depressed patients were more satisfied and were rated as more improved. CONCLUSIONS: Major depression secondary to alcohol dependence that is diagnosed after at least 1 week of abstinence can remain stable in some placebo-treated alcoholics and can respond to desipramine. Treating depression secondary to alcoholism may reduce risk for drinking relapse in some patients. Use of desipramine to reduce relapse in nondepressed alcoholics is not supported.

Adrenergic Uptake Inhibitors↗

PubMed1981

Presynaptic adrenergic receptor sensitivity in depression. The effect of long-term desipramine treatment.

Stimulation of presynaptic alpha 2-adrenergic receptors located on norepinephrine (NE)-containing cells in the brain decreases the firing rate and turnover of NE in these neurons. To assess whether abnormalities in the regulation of the NE system during desipramine hydrochloride treatment may be present in depressed patients, the effects of an alpha 2-agonist, clonidine hydrochloride, on plasma levels of the NE metabolite 3-methoxy-4-hydroxy/phenethyleneglycol (MHPG) and on blood pressure (BP) were evaluated in ten depressed patients before and during long-term desipramine treatment. Long-term desipramine treatment significantly attenuated the effects of clonidine on plasma MHPG level and BP, indicating that during desipramine treatment alpha 2-adrenergic receptors had become subsensitive. In addition, plasma MHPG levels were significantly reduced during long-term desipramine treatment. These findings are discussed in relation to the hypothesized therapeutic mechanism of action of desipramine and the hypotheses relating noradrenergic function and depression.

Adult↗

PubMed1984

Serotonin function and mechanism of action of antidepressant treatment. Effects of amitriptyline and desipramine.

The effects of amitriptyline hydrochloride and desipramine hydrochloride treatment on brain serotonin (5-HT) function were investigated in 21 patients. The ability of an intravenous infusion of the serotonin precursor tryptophan to raise serum prolactin (PRL) levels was determined in 13 depressed patients during placebo administration and after 28 to 35 days of treatment with either amitriptyline or desipramine. Both desipramine (N = 7) and amitriptyline (N = 6) significantly increased the PRL rise induced by tryptophan compared with a preceding placebo period. In contrast, following long-term amitriptyline and desipramine treatment, the ability of tryptophan to increase PRL was enhanced two weeks following abrupt cessation of amitriptyline therapy (N = 5), but not after discontinuation of desipramine therapy. The results of this investigation are consistent with electrophysiologic and behavioral studies in laboratory rats and suggest that desipramine- and amitriptyline-induced alterations in 5-HT function may be related to their antidepressant mechanism of action.

Aged↗

PubMed1989

Desipramine facilitation of initial cocaine abstinence.

We conducted a double-blind, random assignment, six-week comparison of desipramine hydrochloride (n = 24), lithium carbonate (n = 24), and placebo (n = 24) treatments for cocaine dependence. Subjects were 72 outpatient cocaine abusers who met DSM-III-R dependence criteria for cocaine but not for other substance abuse. Subjects in each treatment group were similar in history of cocaine and other substance abuse, cocaine craving, sociodemographics, and other psychiatric comorbidity. Desipramine, compared with both other treatments, substantially decreased cocaine use. Lithium treatment outcome did not differ from that of placebo. Desipramine-treated subjects attained contiguous periods of abstinence substantially more frequently than subjects receiving lithium or placebo. Fifty-nine percent of the desipramine-treated subjects were abstinent for at least three to four consecutive weeks during the six-week study period, compared with 17% for placebo and 25% for lithium. Cocaine craving reductions were also substantially greater in the desipramine-treated subjects. Establishment of initial abstinence is the first stage in recovery from cocaine dependence. Our findings indicate that desipramine is an effective general treatment, for this first treatment stage, in actively cocaine-dependent outpatients.

Adult↗