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PubMed1984

Multicenter double-blind comparison of nomifensine and imipramine for efficacy and safety in depressed outpatients.

Nomifensine, a tetrahydroisoquinoline antidepressant, was compared with imipramine in a 4-week multicenter double-blind study of depressed outpatients (100 on nomifensine, 56 on imipramine). Nomifensine was at least as effective as imipramine in reducing depressive symptoms at average doses of 150 mg/day. When significant differences did occur on Hamilton Depression Rating Scale scores, they favored nomifensine for improvement in cognitive symptoms and interest in work and activities. Early in treatment, nomifensine patients also showed a better relationship between clinical response and side effects. The proportions of patients experiencing at least one side effect or dropping out due to side effects were almost twice as high in the imipramine group. Dry mouth and sedating effects were 2-3 times more frequent among imipramine patients. Thus, nomifensine demonstrated clinical efficacy at least comparable with imipramine but with indications of a more favorable side effects profile.

Adolescent↗
PubMed1984

Halothane-epinephrine arrhythmias and adrenergic responsiveness after chronic imipramine administration in dogs.

The incidence of halothane-epinephrine arrhythmias increases after the short-term administration of imipramine, probably because of enhanced noradrenergic transmission. To determine whether this effect persists after long-term imipramine treatment, we have studied the arrhythmogenicity and adrenergic responsiveness in halothane anesthetized dogs after six weeks of imipramine administration, 150 mg X day-1, orally. The mean (+/- SD) arrhythmogenic dose of epinephrine (ADE) in nine dogs anesthetized with 1.2 MAC halothane was 2.57 (+/- 1.04) micrograms X kg-1 X min-1. The alpha-adrenergic responsiveness, assessed as the dose of phenylephrine that caused a 75% increase in mean arterial pressure (alpha 75), was 5.78 +/- 2.39 micrograms X kg-1 X min-1. The dose of isoproterenol that increased heart rate by 75% (beta 75) was 309 +/- 180 ng X kg-1 X min-1. After imipramine treatment, the ADE (2.63 +/- 1.26), alpha 75 (5.16 +/- 2.05), and beta 75 (386 +/- 266) were not statistically different from the pre-imipramine values (P greater than 0.05), despite a fivefold increase in circulating norepinephrine. We conclude that chronic imipramine does not alter arrhythmogenicity and adrenergic responsiveness, since compensatory mechanisms, at the sympathetic nerve terminal, may revert the initial hyper-responsiveness to normal.

Anesthesia↗
PubMed1982

[Effects of thymo-analeptics and acceptability of amineptin compared to those of imipramine].

Amineptine and imipramine were compared in a double-blind controlled trial carried out in 52 depressed patients over a period of 30 days, with daily doses of amineptine ranging from 100 to 300 mg or of imipramine ranging from 50 to 150 mg. Global assessment of response to treatment and Hamilton rating scale scores showed no significant difference between amineptine and imipramine. Both drugs were effective as soon as the 7th day of treatment, and their efficacy constantly increased during the 30 days of the observation. The clinical acceptability of amineptine is superior to that of imipramine: in the amineptine group acceptability was considered excellent in 67% of the cases; in the imipramine group acceptability was considered excellent in 48%. 8% of the patients in the imipramine group were withdrawn from the trial because of intolerance.

Adolescent↗
PubMed1994

Neuroanatomical specificity and dose dependence in the time course of imipramine-induced beta adrenergic receptor down-regulation in rat brain.

The time course of beta adrenergic receptor adaptation in response to chronic imipramine treatment (10 or 20 mg/kg) was assessed by quantitative autoradiographic analysis of 125I-pindolol binding in rat brain. Binding of the radioligand was assessed in 18 brain areas, including subregions of the hippocampus, amygdala, septum, hypothalamus and specific cerebral cortical regions. After only 2 days treatment with imipramine at a dose of 20 mg/kg, select cortical regions exhibited a reduction in 125I-pindolol binding. These rapidly adapting cortical regions included the medial prefrontal, lateral frontal, ventrolateral orbital and piriform cortices. After 7 or 21 days treatment with imipramine at 20 mg/kg, 16 of 18 brain regions examined exhibited significant reduction in 125I-pindolol binding. The only regions examined that did not show reduced 125I-pindolol binding for these treatment conditions were the caudate-putamen and anterior hypothalamic area. After 2 days treatment with 10 mg/kg of imipramine, down-regulation of beta adrenergic receptors was not observed in any region. After 7 days treatment with 10 mg/kg, down-regulation of beta adrenergic receptor binding was found only in certain cortical regions: medial prefrontal, lateral frontal, ventrolateral orbital and piriform cortices. Thus, the cortical regions that were most rapidly affected with the 20 mg/kg dose of imipramine (i.e., after 2 days) were also the first to respond with the 10 mg/kg dose of the drug. After 21 days treatment with imipramine at 10 mg/kg, 125I-pindolol binding was reduced in 13 of the 18 regions examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Subacute imipramine: changes in single dose pharmacokinetics in rats.

Imipramine (10 mg/kg, p.o.) administered to male Wistar rats (133-178 g) twice daily for 3 weeks more than halved the control rate of body weight gain. A bile fistula was inserted after this period and 14C-imipramine (10 mg/kg, p.o.) was administered 14-18 hr after the final scheduled dose. Biliary excretion of radioactivity during the subsequent 50 min was decreased to 16% of control. Higher levels of gastrointestinal radioactivity (mainly in the stomach lumen) indicated a slower imipramine absorption rate in the subacute group. Liver metabolite ratios revealed that the treatment group had decreased rates of 2-hydroxylation and 10-hydroxylation, but not demethylation, of imipramine. After incubation of the 25-50 min bile sample with glusulase, bile-to-liver ratios of metabolites indicated a lower entry rate of imipramine, desmethylimipramine and 2-hydroxydesmethylimipramine, but not of 2-hydroxyimipramine or 10-hydroxyimipramine, into bile of the subacute imipramine group.

Administration, Oral↗
PubMed1996

Responders to antidepressant drug treatment: a study comparing nefazodone, imipramine, and placebo in patients with major depression.

BACKGROUND: Nefazodone hydrochloride, an antidepressant that acts as a 5-HT2 antagonist and serotonin (5-HT) and norepinephrine uptake inhibitor, was evaluated in a double-blind, imipramine- and placebo-controlled study involving 128 patients with major depression. METHOD: Eligible patients were randomly assigned to receive placebo (2 to 6 capsules/day), imipramine (100 to 300 mg/day), or nefazodone (200 to 600 mg/day) for 8 weeks. The principal efficacy outcome measure assessed was the number of patients who experienced an adequate response during treatment. RESULTS: Based on global improvement (Clinical Global Impressions-Improvement), 67% of nefazodone-treated patients (p < or = .01) and 63% of imipramine-treated patients (p < or = .05) responded during 8 weeks of treatment, compared with 36% of placebo controls. Sixty-two percent of nefazodone-treated, 53% of imipramine-treated, and 26% of placebo-treated patients had 17-item Hamilton Rating Scale for Depression (HAM-D-17) scores < or = 10 on completion of acute treatment. Nefazodone-treated patients had a lower incidence of premature treatment discontinuation and fewer dropouts for adverse events than the imipramine group. CONCLUSION: In a three arm comparison with imipramine and placebo, nefazodone had the greatest number of patients with major depression who responded to therapy. Nefazodone, a new antidepressant with novel pharmacology, is a well-tolerated, efficacious antidepressant.

Adult↗
PubMedDate not supplied

The pharmacokinetics of promazine and its metabolites after acute and chronic administration to rats--a comparison with the pharmacokinetics of imipramine.

This study was aimed to investigate the pharmacokinetics of promazine (a phenothiazine analogue of imipramine) after its single and repeated administration. Male Wistar rats received promazine as a single injection (10 mg/kg ip) or they were treated chronically with the neuroleptic, once a day for two weeks. Plasma and brain concentration of promazine, desmethylpromazine and promazine sulphoxide were determined using the HPLC method devised by us. The results of the present study were compared with our earlier data obtained in analogous experiments with imipramine. The obtained data showed that the pharmacokinetics of promazine and imipramine was similar, though certain differences could be noticed. Both those drugs were unevenly distributed throughout the body, occurring in low concentrations in the blood plasma and reaching considerably higher concentrations in the brain. However, the uptake of promazine by the brain was more efficient than that of imipramine. The brain/plasma AUC ratio after a single dose amounted to 28.72 for promazine and 12.78 for imipramine. Their demethylated metabolites behaved in a similar way, where as the level of promazine sulphoxide in the brain was three times lower than that in the plasma. Chronic treatment with promazine or imipramine increased concentrations of the parent compounds and their demethylated metabolites, and prolonged their half-life in the plasma and brain. The plasma level of promazine sulphoxide did not change, and its brain level was decreased by chronic treatment with promazine. The half-life of promazine sulphoxide was prolonged in the plasma but shortened in the brain after repeated administration of promazine. The observed considerable amounts of desmethylpromazine and promazine sulphoxide, formed in vivo, suggest that the two compounds are major metabolites of promazine, and that the metabolic pattern of promazine in the rat and man is similar.

Animals↗
PubMed1996

Paroxetine in the treatment of Chinese patients with depressive episode: a double-blind randomized comparison with imipramine.

BACKGROUND: Paroxetine is a potent inhibitor of serotonin re-uptake. Although it has been widely used as an antidepressant in western countries, its efficacy and side effects in the Chinese are unknown. METHODS: Patients with major depressive episode were recruited from the outpatient clinic and the acute wards of the Department of Psychiatry, Veterans General Hospital-Taipei in 1994. Severity of depression was evaluated with Hamilton Rating Scale for Depression (HAM-D), Clinical Global Impression (CGI) and the adverse effects were evaluated with Treatment Emergent Symptom Scale (TESS). Forty Chinese patients with HAM-D scores > or = 18 at the beginning of the first dose were randomized to receive paroxetine (20 to 30 mg/day) or imipramine (100 to 125 mg/day). The dosage was designed as a fixed-adjustable regimen for an active treatment period of six weeks. The patients and the clinical investigators were both blind to the medication until the end of the trial. RESULTS: Five patients violating the trial protocol were excluded from this study, leaving 35 patients for efficacy and adverse effect analyses. Sixty-seven percent (12/18) of paroxetine-treated patients and 65% (11/17) of imipramine-treated patients showed a 50% or more reduction in HAM-D scores. The rate of patients whose mood recovered to normal or near-normal (borderline) was higher in the paroxetine group (66.7%) than in the imipramine group (35.3%), but the difference was not statistically significant (p = 0.13). At the end of this trial, the mean reduction of HAM-D scores was similar between groups (20.2 +/- 9.1 vs 15.3 +/- 8.4, p > 0.1). Three patients in the paroxetine group and two patients in the imipramine group withdrew prematurely due to adverse effects of impatience. Adverse effects of anticholinergic effects were reported more frequently in the imipramine group than in the paroxetine group (p = 0.01). CONCLUSIONS: In comparison with imipramine, paroxetine affords fewer anticholinergic adverse effects without the sacrifice of efficacy in the treatment of depressed Chinese patients.

Adult↗
PubMed1977

Chemiluminescence resulting from an interaction between imipramine and human polymorphonuclear leukocytes.

The addition of imipramine to a suspension of resting polymorphonuclear leukocytes (PMNs) resulted in the generation of chemiluminescence (CL) (100,000 cpm with 1 X 10(-4)M imipramine). In the presence of a particle (zymosan) capable of activating the PMNs to generate reactive oxygen species, the magnitude of CL observed with 1 X 10(4)M imipramine was greatly enhanced (greater than 1,000,000 cpm). No CL was detected upon the addition of imipramine to PMNs isolated from a chronic granulomatous child or to alveolar macrophages isolated from rats. Another tricyclic antidepressant, amitriptyline, failed to generate CL with PMNs either alone or in the presence of zymosan; however, both imipramine and amitriptyline generated CL upon addition to the xanthine oxidase-purine superoxide generating system. Although the mechanism by which this drug-cell interaction results in the generation of CL is not known, the observations are suggestive that the CL may originate, in part, from the activation of imipramine by some reactive oxygen state(s).

Amitriptyline↗
PubMed1996

Prolonged P300 latency in attention deficit hyperactivity disorder predicts poor response to imipramine.

P300 is a cognitive evoked potential that evaluates attention and information processing. This study uses auditory and visual P300 topography to develop a classification of attention deficit hyperactivity disorder (ADHD), and find predictors of treatment response. Of 45 ADHD children ages 6 to 15 treated with pemoline in a previous study, 25 were poor responders. Of these 25, 17 participated in an imipramine treatment protocol. Auditory and visual P300 testing was performed before and after treatment using 31 scalp electrodes. Good and poor responders to imipramine were clinically identical. Poor imipramine responders had longer auditory and visual P300 latencies than good responders. Treatment with imipramine decreased auditory P300 latencies and increased auditory P300 amplitudes. We have previously reported that ADHD patients with small right frontocentral auditory P300 amplitudes respond poorly to pemoline. Thus, P300 topography and latency classifies ADHD into three groups: group 1 with normal P300 topography, and good response to pemoline; group 2 with small right frontocentral auditory P300 amplitudes, poor response to pemoline, and good response to imipramine; and group 3 with long auditory and visual P300 latencies and small right frontocentral auditory P300 amplitudes, and poor response to pemoline and imipramine.

Adolescent↗
PubMed1985

High and low affinity [3H]imipramine binding sites in control and parkinsonian brains.

[3H]Imipramine binding was studied in the prefrontal cortex and putamen of post-mortem brains from control and Parkinsonian subjects. Saturation and inhibition curves showed both high affinity [3H]imipramine binding related to the serotonin uptake mechanism and low affinity binding which was sodium-independent and unrelated to serotonergic uptake. After subcellular fractionation, high affinity [3H]imipramine binding sites were enriched in synaptosomal fractions. In Parkinson's disease, where brain serotonin concentrations are decreased, there was a significant reduction in the density of the high affinity binding in the prefrontal cortex and putamen while the characteristics of the low affinity binding sites remained unchanged. After subcellular fractionation of the putamen of Parkinsonian patients, the decrease in [3H]imipramine binding was found predominantly in the synaptosomal fractions. These results are consistent with a relation between the high affinity [3H]imipramine binding sites and the neuronal serotonin uptake mechanism. Estimation of [3H]imipramine binding could be used as a specific marker for the study of serotonergic innervation in human post-mortem material. The reduction in the density of tricyclic antidepressant binding sites found in cortical and subcortical areas of Parkinsonian brains may be somehow implicated in the depression often seen in patients.

Aged↗
PubMed1983

Localization of [3H]-imipramine binding sites in rat brain by light microscopic autoradiography.

The binding characteristics of [3H]-imipramine in slide mounted tissue sections of rat forebrain have been studied to ascertain the optimal binding conditions for labeling the sites prior to autoradiographic localization. The conditions for the experiments and the kinetics of the imipramine binding correspond reasonably well with those used in membrane preparations to initially define the imipramine binding site. Subsequent labeling of sections, using these parameters, allowed the autoradiographic localization of high concentrations of imipramine binding sites in such areas as the cerebral cortex, striatum, and several limbic and visual system structures. In addition, there was a marked overlap between regions demonstrating imipramine binding and areas known to be innervated by serotonergic neurons. This study outlines the potential sites of action of imipramine in the brain and defines areas for future investigations which attempt to localize brain regions involved in the etiology of depression and areas involved in the side effects of antidepressant drug therapy.

Animals↗
PubMed1998

Imipramine does not affect argon-laser-induced pin-prick pain thresholds and laser-evoked cerebral potentials.

The tricyclic antidepressant imipramine has shown analgesic effect in human clinical and experimental pain studies. The aim of the present study was to test the effect of imipramine on a pure short-term nociceptive stimulus with pin-prick pain quality. In a randomized, placebo-controlled, double-blind, crossover study, the hypoalgesic effect of a single oral dose of 100 mg imipramine was investigated in 10 healthy volunteers. Test procedures performed before and 2, 4, 6, 8, 10, 12 and 14 h after medication included determination of warmth and pin-prick pain thresholds to high-energy argon laser light stimulation on the hand, as well as laser-evoked cerebral potentials to suprathreshold stimulation. Both the warmth and the pin-prick pain thresholds (p=0.49 and 0.85) and the root mean square of the laser-evoked potentials (p=0.89) were unaltered by imipramine. It is concluded that a single oral dose of 100 mg imipramine has no effect on pin-prick pain. This study demonstrates the important fact that a drug may show clear analgesic effect in some experimental pain models while it is without effect in other models; e.g. imipramine is known to affect pain tolerance and summation thresholds. Pre-clinical tests of potentially analgesic drugs should therefore be based on different pain-stimulation modalities. Copyright 1998 European Federation of Chapters of the International Association for the Study of Pain.

Journal Article↗
PubMed1985

Effects of neonatal antithyroid treatment on brain [3H]-imipramine binding sites.

The action of the antithyroid, sulphydryl reagent methimazole (MMI) on the specific binding of [3H]-imipramine in the cerebral cortex and corpus striatum of immature and mature rats has been examined. Chronic administration of MMI through the first 30 days of life decreased the number of imipramine binding sites in cortical but not striatal membranes, as assessed 48 h after the last injection of goitrogen. A similar treatment did not affect the binding profile of [3H]-imipramine in mature rats. Acute administration of MMI to 30 day-old rats increased the number of imipramine binding sites shortly after the injection, an effect no longer evident 48 h later. MMI in vitro increased the binding of [3H]-imipramine. It is concluded that maturational impairment of the hypothyroid cortex, rather than any alteration of membrane bound thiol groups, was a major cause for the diminished binding of [3H]-imipramine in MMI-treated, immature rats.

Aging↗
PubMed1985

Relationship between levels and uptake of serotonin and high affinity [3H]imipramine recognition sites in the rat brain.

High affinity [3H]imipramine binding, endogenous levels of serotonin and noradrenaline, and serotonin uptake were determined in brain regions of rats with selective destruction of serotonergic neurons by 5,7-dihydroxytryptamine (5,7-DHT), of adrenergic neurons by 6-hydroxydopamine (6-OHDA), and of rats treated with reserpine. Neonatal treatment with 5,7-DHT resulted in a significant decrease of both serotonin levels and density (Bmax) of high affinity [3H]imipramine binding sites in the hippocampus. In contrast, an elevation of serotonin levels and an increase in Bmax of [3H]imipramine binding were noted in the pons--medulla region. No changes were observed in the noradrenaline content in either of these regions. Intracerebral 6-OHDA lesion produced a drastic suppression of noradrenaline levels in cerebral cortex but failed to alter the binding affinity (KD) or density (Bmax) of [3H]imipramine recognition sites. A single injection of reserpine (2.5 mg/kg) resulted in marked depletion of both serotonin (by 57%) and noradrenaline (by 86%) content and serotonin uptake (by 87%) in the cerebral cortex but had no significant influence of the parameters of high affinity [3H]imipramine binding in this brain region. The results suggest that high affinity [3H]imipramine binding in the brain is directly related to the integrity of serotonergic neurons but not to the magnitude of the uptake or the endogenous levels of the transmitter, and is not affected by damage to noradrenergic neurons or by low levels of noradrenaline.

5,7-Dihydroxytryptamine↗
PubMed1963

THE INCREASE IN THE TOXICITY OF YOHIMBINE INDUCED BY IMIPRAMINE AND OTHER DRUGS IN MICE.

In mice, yohimbine appears to accentuate the normal "alarm" reactions (alerting, flight) to external stimuli. Imipramine increases this effect and at the same time converts a non-lethal dose of yohimbine into a lethal one. The effect of imipramine is greatly reduced by adrenalectomy or by treatment with reserpine, syrosingopine, ganglion-blocking drugs or adrenaline antagonists acting on sympathetic beta-receptors. Hypnotic, anti-convulsant or anaesthetic agents, tetrabenazine or antagonists of 5-hydroxytryptamine do not reduce the imipramine effect. A variety of drugs which, like imipramine, are known to interfere with the tissue binding of noradrenaline also increase the toxicity of yohimbine. Yohimbine significantly reduces brain noradrenaline content; adrenal catechol amines are slightly reduced. The results suggest that yohimbine releases noradrenaline from stores or nerves as a consequence of increased central sympathetic activity. Imipramine increases the actions and toxicity of yohimbine by increasing the effects of the released noradrenaline on beta-receptors. The lethal effects of a high dose of yohimbine alone are not reduced by any of the treatments tested, and appear not to result from activation of sympathetic mechanisms.

Adrenal Glands↗
PubMed1978

Behavior therapy, supportive psychotherapy, imipramine, and phobias.

In a controlled outcome study of phobias, 111 adult patients (69% women, 31% men) received a course of 26 weekly treatment sessions consisting of (1) behavior therapy and imipramine hydrochloride (2) behavior therapy and placebo, or (3) supportive psychotherapy and imipramine. Patients were classified as agoraphobic, mixed phobic, or simple phobic. The great majority of patients in all groups showed moderate to marked global improvement (70% to 86%, depending on rater). In agoraphobics and mixed phobics (both groups experiencing spontaneous panic attacks), imipramine was significantly superior to placebo. There was no difference between behavior therapy and supportive therapy, both resulting in high improvement rates (76% to 100%, depending on rater). In simple phobic patients, there was a high rate of improvement with all treatment regimens (72% to 93%, depending on rater), with no significant difference between imipramine and placebo or between behavior therapy and supportive therapy. Of 88 moderately to markedly improved patients followed up for one year after completing treatment, 83% maintained their gains and 17% relapsed. No patients showed symptom substitution. Eighteen percent of the patients receiving imipramine hydrochloride showed marked stimulant side effects on from 5 to 75 mg/day.

Adult↗
PubMed1978

Imipramine and desipramine in plasma and spinal fluid: relationship to clinical response and serotonin metabolism.

In a double-blind study of depressed patients treated with imipramine hydrochloride, levels of imipramine and desipramine were measured in plasma and in CSF. Levels of both drugs in CSF were approximately 10% of plasma levels, but the levels in the two body fluids were highly correlated. The levels of both drugs were approximately equal in plasma, but desipramine predominated in CSF (imipramine/desipramine ratio of 0.8). The imipramine-induced alteration in CSF levels of the serotonin metabolite (5-hydroxy-indoleacetic acid [5HIAA]) correlated with imipramine levels but not with desipramine. For the group of patients showing a clear antidepressant response, the mean drug levels were nearly double those of the nonresponder group, a difference that did not quite reach statistical significance in this relatively small sample. The desipramine levels showed no responder-nonresponder difference, while the ratio of imipramine/desipramine was significantly higher among the responders. On the average this particular patient group had relatively low pretreatment levels of 5HIAA in CSF, an observation that may partially account for the relatively low overall response rate to imipramine.

Adult↗