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PubMed1977

In vitro effects of imipramine on proliferation of human leukocytes.

The effects of imipramine hydrochloride on cell proliferation were investigated in leukocyte cultures derived from normal volunteers. Nine different doses of imipramine were added in vitro at random for 4, 24, 48, and 68 hours, the three lowest concentrations being within the range of plasma levels reported in psychiatric patients receiving the drug therapeutically. Cell proliferations, as measured by mitotic index, was affected by both the concentration and the duration of drug exposure; the higher the dose and/or the longer the drug in culture, the lower the mitotic index. Imipramine concentrations corresponding to therapeutic plasma levels had no effect on mitotic index regardless of the length of exposure.

Adult↗
PubMed1983

Imipramine as treatment for depression in addicts.

This report describes the results of a placebo-controlled double-blind clinical trial evaluating imipramine hydrochloride, a tricyclic antidepressant, as treatment for depression in methadone-maintained opiate addicts. Forty-six subjects were assigned randomly to either the imipramine or placebo group for up to eight weeks. All patients also received mandatory once weekly group therapy as part of the methadone program. Outcome measures included attrition, depressive symptoms, global improvement, side effects, social functioning, and urine specimen results positive for illicit drugs. The therapeutic response in the two conditions was similar. Addicts receiving either imipramine or placebo experienced a substantial reduction of depressive symptoms during the eight weeks of the study. These findings are compared with other studies that treat depression in addicts and nonaddicts.

Adult↗
PubMed1987

Platelet tritiated imipramine binding and serotonin uptake in depressed patients and controls. Relationship to plasma cortisol levels before and after dexamethasone administration.

We measured platelet tritiated imipramine binding and serotonin uptake in 51 depressed patients and 43 normal controls. Although there were no significant differences in platelet 3H-imipramine binding or serotonin uptake when the total group of depressed patients was compared with controls, depressed women (n = 32) had a significantly lower maximal density of 3H-imipramine binding sites (beta max) than control women (n = 25). Moreover, among the total group of depressed patients, there were significant negative correlations between the beta max values and plasma cortisol levels at 4 PM (n = 41) and 11 PM (n = 41) following dexamethasone administration. These negative correlations between beta max and cortisol levels were strongest among melancholic patients both at 4 PM before dexamethasone administration (n = 14) and at 11 PM after dexamethasone administration (n = 15). These data suggest that the reported decrease in beta max found among depressed patients may be related to and is perhaps secondary to the hypercortisolemia of depression.

Adult↗
PubMed1987

Adjunctive imipramine in the treatment of postpsychotic depression. A controlled trial.

The efficacy of adjunctive imipramine hydrochloride treatment for syndromally defined postpsychotic depression was assessed in a six-week, double-blind, placebo-controlled study. All patients had been diagnosed as having schizophrenia or schizoaffective disorder, all were receiving stable doses of fluphenazine decanoate, and all had received benztropine mesylate in an attempt to rule out neuroleptic-induced akinesia. Patients randomized to imipramine therapy fared significantly better in terms of their global improvement and in terms of individual symptoms that are components of the depression syndrome. There were no significant differences in outcome psychosis ratings or side effects. This study indicates the existence of an identifiable syndrome of secondary depression in this patient group that is likely to respond favorably to treatment with adjunctive imipramine.

Adult↗
PubMed1988

Imipramine treatment for chronic depression.

Antidepressant drugs in the treatment of chronic depressions have received little systematic study. We used a two-week, single-blind placebo washout followed by a six-week, double-blind comparison of imipramine hydrochloride and placebo in a sample of 76 outpatients with DSM-III dysthymic disorder entered into a trial at two centers. Subjects were preponderantly female, had insidious onset at an early age, and had depressions of moderate severity; 96% also met the DSM-III criteria for major depressive disorder at the time of presentation. Sixty percent had a history of persistent depressive symptoms sufficient to meet criteria for major depression for longer than two years. Markedly favorable responses occurred in 45% of imipramine-treated (n = 29) and 12% of placebo-treated (n = 25) patients and, respectively, 59% and 13% of those who completed the study. Imipramine produced significant advantage in measures of depressive symptoms, global severity of illness, and self-rated social and vocational function. Recovered patients experienced remission from both long-standing symptoms and deficits as well as more recently exacerbated aspects of their syndrome. Patients with pure dysthymic disorder of a mild, subsyndromal type were uncommon in these clinical settings. However, anti-depressant medication was effective for many moderately severe chronic depressions, which had previously been untreated or undertreated, presumably related to misdiagnosis.

Adult↗
PubMed1989

Imipramine dose-response relationship in panic disorder with agoraphobia. Preliminary findings.

At the end of a two-week single-blind placebo baseline, 43 patients with a diagnosis of panic disorder with agoraphobia without significant dysphoria-depression and with moderate to severe panic and phobic symptoms were assigned to, and 32 of them completed, a placebo-controlled (n = 7) dose-response study with three weight-adjusted imipramine hydrochloride dosages: 0.5 mg/kg/d (n = 10), 1.5 mg/kg/d (n = 9), and 3 mg/kg/d (n = 6). Eleven patients, three from the medium-dose and eight from the high-dose conditions, dropped out owing to side effects. No instructions or encouragement for self-directed exposure to phobic situations or other coping strategies with panic or fear were given throughout the trial. Compliance, as assessed by pill counts and by plasma tricyclic levels, was high. Results provided strong evidence for a positive dose-response relationship on panic and phobic symptoms and confirmed earlier suggestions (1) that imipramine without concurrent exposure possesses a significant antipanic and antiphobic effect, (2) that improvement correlates primarily with imipramine but not N-desmethylimipramine plasma levels, and (3) that side effects prevent optimum dose buildup in a substantial proportion of patients with this disorder.

Adolescent↗
PubMed1993

Maintenance drug treatment of panic disorder. I. Results of a prospective, placebo-controlled comparison of alprazolam and imipramine.

One hundred six patients diagnosed according to DSM-III as suffering from agoraphobia with panic disorder, panic disorder with limited phobic avoidance, or uncomplicated panic disorder entered an acute 8-week treatment phase. Patients who improved received an additional 6 months' maintenance treatment. Significantly more patients treated with alprazolam than with imipramine hydrochloride or placebo remained in therapy and experienced panic attack and phobia relief during the acute treatment phase. During the maintenance phase, neither tolerance nor daily dose increase was observed. All patients who completed the maintenance phase (27 in the alprazolam group, 11 in the imipramine group, and 10 in the placebo group) were panic free at the end of 8 months of study treatment. Alprazolam therapy was effective and well tolerated at a mean daily dose of 5.7 mg. Imipramine hydrochloride (175 mg/d) also produced significant panic relief but was associated with poor patient acceptance.

Adult↗
PubMed1994

Maintenance imipramine therapy for secondary depression in schizophrenia. A controlled trial.

BACKGROUND: Although recent studies have documented the benefit of adjunctive antidepressant medication for the short-term treatment of certain patients with operationally defined syndromes of postpsychotic depression, the value of maintenance adjunctive antidepressant treatment in this circumstance has not been properly established. METHODS: This study examined 24 schizophrenic or schizoaffective patients with postpsychotic depression or negative symptoms. These patients had all been benefited over the short term by the addition of adjunctive imipramine hydrochloride to their ongoing fluphenazine decanoate/benztropine mesylate regimens, and this adjunctive treatment had been successfully continued for 6 months. In a randomized double-blind protocol, treatment with adjunctive imipramine hydrochloride (mean, 233 +/- 72 mg/d) was then either maintained or tapered to placebo for an ensuing 1-year trial, while treatment with fluphenazine and benztropine continued. RESULTS: Significantly more patients who received placebo substitution relapsed into depression (P < .001). Patients who received placebo substitution were also more likely to experience relapses into psychosis (P < .02). CONCLUSIONS: These results support the clinical value of maintenance adjunctive imipramine therapy among initially responsive patients with postpsychotic depressions.

Adult↗
PubMed1994

A double-blind placebo-controlled comparison of phenelzine and imipramine in the treatment of bulimia in atypical depressives.

Although antidepressants have been found to be superior to placebo in 12 of 14 studies, the relationship between improvement in the depressive diathesis and bulimia is unclear. In this study, the efficacy of placebo, imipramine, and phenelzine is examined in patients comorbid for atypical depression and bulimia. Greater improvement was observed for both depressive and bulimic symptoms with phenelzine than with either imipramine or placebo. Consistent with its poor antidepressant effects in atypical depression, imipramine seemed to have minimal efficacy for the bulimic symptoms of atypical depressives. These data suggest that the presence of bulimia does not alter the treatment response of atypically depressed patients. Furthermore, the data may suggest a link between depression and bulimia in atypical depressives. Demonstrating a statistical difference with a small sample suggests the effect size is robust, however conclusions are limited by a small sample size.

Adult↗
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↗
PubMed1977

Impurities in drugs I: Imipramine, desipramine, and their formulations.

Nineteen lots of imipramine tablets and four lots of desipramine tablets were examined for impurities by TLC. Iminodibenzyl, desipramine, and 10,11-dihydro-5-[3-(methylamino-3'-dimethylaminopropyl)propyl]-5H-dibenz[b,f]azepine dihydrobromide (I) were found in some imipramine tablets, and iminodibenzyl and imipramine were found in some desipramine tablets, all at levels of less than 0.3% of label claim of the drug. Except for I, the identity of the impurities was established by comparison with known standards; I was synthesized and its composition was established by elemental analysis. All impurities, including I, were characterized by TLC, GLC, and mass spectrometry.

Capsules↗
PubMed1982

GLC method for iminodibenzyl and desipramine impurities in imipramine hydrochloride and its formulated products.

A GLC method is described for the determination of iminodibenzyl and desipramine impurities in imipramine hydrochloride and its formulated products. These impurities were extracted from an alkaline solution with a mixture of 30% methylene chloride in hexane for chromatography on a 3% OV-17 GLC column. Iminodibenzyl was determined using anthracene as an internal standard and desipramine was determined (after derivatization) using nortriptyline as an internal standard. Based on spiked excipient mixtures typically used to compound imipramine tablets, recoveries were 93-109% for iminodibenzyl and 93-107% for desipramine at 0.2-0.4% of the labeled claim of imipramine. Minimum detection levels were approximately 0.02% for each impurity, and procedural standards gave coefficients of variation of less than 1% for each impurity. The method was linear in the 0.05-0.5 microgram range and typically gave correlation coefficients greater than or equal to 0.999.

Amines↗
PubMed2002

Chronic treatment with imipramine or mirtazapine antagonizes stress- and FG7142-induced increase in cortical norepinephrine output in freely moving rats.

The effect of repeated administration of imipramine or mirtazapine, two antidepressant drugs with different mechanisms of action, was studied on the stress-induced increase in the extracellular concentration of norepinephrine in the prefrontal cortex of freely moving rats. Exposure to footshock in control rats induced a marked increase in extracellular norepinephrine concentrations in the prefrontal cortex (+120%). Long-term administration with imipramine or mirtazapine (10 mg/kg, i.p., twice or once a day, respectively, for 14 days) reduced (+50%) the effect of stress on basal norepinephrine output. Acute administration of FG7142 (30 mg/kg, i.p.), an anxiogenic benzodiazepine receptor inverse agonist, induced a marked increase in norepinephrine output (+90%) in control rats. In rats chronically treated with imipramine or mirtazapine this effect was completely antagonized. On the contrary, acute administration of these antidepressant drugs failed to reduce stress- and FG7142-induced increase in norepinephrine output. The plastic changes in the sensitivity of norepinephrine neurons to footshock stress and drug-induced anxiogenic stimuli may reveal a new important neuronal mechanism involved in the long-term modulation of emotional state. This action might be relevant for the anxiolytic and antidepressant effect of antidepressant drugs.

Animals↗
PubMed1994

In vivo biogenic amine efflux in medial prefrontal cortex with imipramine, fluoxetine, and fluvoxamine.

In vivo brain microdialysis was used to determine the effects of the standard tricyclic antidepressant imipramine and the two selective serotonin reuptake inhibitors (SSRIs) antidepressants, fluoxetine and fluvoxamine, on extracellular levels of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) in rat medial prefrontal cortex. When given intraperitoneally (IP), imipramine increased NE in the microdialysis perfusate, and elevated DA and 5-HT to a lesser extent. Similar dose-dependent increases in DA and 5-HT were detected after IP fluoxetine, although NE was less affected. In contrast, IP fluvoxamine produced no change in basal NE nor DA, although a large increase in 5-HT occurred at an intermediate dose. When administered directly into cortex, all three antidepressants increased 5-HT by the same amount in a dose-dependent fashion. Intracortical imipramine and fluoxetine increased NE, and fluoxetine and fluvoxamine both increased DA, with fluoxetine doing so at a lower concentration. These data suggest that the SSRIs are not entirely selective for serotonin in vivo.

Animals↗
PubMed1997

The effect of prolonged imipramine treatment on the alpha 1-adrenoceptor-induced translocation of protein kinase C in the central nervous system in rats.

The aim of the study was to investigate the effects of prolonged treatment with imipramine (10 mg kg-1/day i.p. for 21 days) on the translocation of protein kinase C (PKC) after stimulation of the alpha 1-adrenoceptor. Methoxamine (5-50 mg kg-1) and phenylephrine (0.1-1 mg kg-1) induced a rapid and long-term redistribution of PKC from the cytosolic to the membrane fraction in the rat frontal cortex and hippocampus. The effects of methoxamine and phenylephrine were completely blocked by pretreatment with prazosin. Prolonged pretreatment with imipramine changed the response of PKC to methoxamine and phenylephrine. Much lower doses of alpha 1-adrenoceptor agonists were able to induce the redistribution of PKC. Moreover, prolonged treatment with imipramine markedly increased the basal activity of PKC in the membrane fractions of the frontal cortex and hippocampus.

Animals↗
PubMed1978

Comparative cardiovascular toxicity of trazodone and imipramine in the rat.

Several authors have associated the cardiotoxicity of the tricyclic antidepressants with their capacity to potentiate the response to catecholamines. Trazodone is a psychotropic drug with a clinically proven antidepressant activity. It differes from the tricyclic antidepressants under several aspects (chemistry, pharmacology, mode and mechanism of action, etc.), including interactions with catecholamines. Contrary to the tricyclic antidepressants, it does not potentiate the response to catecholamines, but, instead, has an adrenolytic activity. We therefore decided to compare the cardiotoxicity of trazodone and of a tricyclic antidepressant, i.e. imipramine in the rat. The experiments were conducted on anaesthetized Long Evans rats, the drugs being administered by i.v. infusion until cardiac arrest occurred; ECG (lead II) and blood pressure (BP) were recorded at the same time. The primary effect of trazodone was its hypotensive action. ECG changes, consisting of a lengthening of the PR interval, were observed only when there was a marked drop in BP. The primary effect of imipramine, instead, consisted of disturbances in cardiac conduction. It is concluded that trazodone and imipramine produce different cardiovascular effects.

Animals↗
PubMed1991

Effects of imipramine and some tryptamine derivatives on the efflux of 3H-5-hydroxytryptamine from rabbit platelets.

The efflux of 3H-5-hydroxytryptamine (3H-5-HT) from rabbit platelets (monoamine oxidase inhibited; pretreatment with reserpine) was measured in the absence and presence of various concentrations of imipramine or a number of tryptamine derivatives. The maximum efflux-accelerating effect (Emax) of 5-HT and some other tryptamines (e.g., N-methyl-5-HT, 5-methoxytryptamine) far exceeded that of imipramine, whereas the Emax for 2-methyl-5-HT did not. It is concluded that tryptamines that are more effective in releasing 3H-5-HT than imipramine have the property of being substrates of the 5-HT transporter.

Analysis of Variance↗
PubMed1993

Use-dependent effects of acute and chronic treatment with imipramine and buspirone on excitatory synaptic transmission in the rat hippocampus in vivo.

The effects of acute and long-term treatment with imipramine and buspirone on the responses of rat hippocampal neurones to low and high frequency electrical stimulation were compared. Whereas acute treatment with imipramine (10 mg/kg, i.p.) had no effect on synaptic responses to low frequency stimulation, chronic treatment for 14 days significantly reduced the amplitude of the field excitatory postsynaptic potential. Both acute and chronic imipramine treatment markedly reduced the amplitude of the nerve volley and excitatory postsynaptic potential evoked at high frequency stimulation rates in a use-dependent manner. Buspirone (0.5-3 mg/kg, i.p.) produced a significant reduction of the excitatory postsynaptic potential at high frequencies. This was enhanced after repeated administration of a dose of 0.5 mg/kg for 14 days. We previously reported a similar effect of buspirone at low frequency stimulation. Both compounds therefore share the ability to exert strong depressant effects on transmission in the hippocampus especially after chronic treatment.

Animals↗