Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “IMIPRAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 289 records · Page 16Linked to original sources
PubMed1994

Comparison of venlafaxine and imipramine in the acute treatment of major depression in outpatients.

BACKGROUND: Venlafaxine is a new phenylethylamine antidepressant that exhibits monoamine reuptake inhibition. The current study evaluates the efficacy of venlafaxine compared to that of imipramine in outpatients suffering from major depression of moderate-to-marked severity. METHOD: We conducted a double-blind, placebo-controlled, 6-week treatment study of 224 outpatients who met DSM-III-R criteria for major depression, and who had a score of at least 20 on the 21-item Hamilton Rating Scale for Depression (HAM-D). Dosage was flexible and administered on a three-times-a-day schedule, with a mean maximum daily dose of 182 mg for venlafaxine and 176 mg for imipramine. RESULTS: For patients completing 6 weeks of treatment with venlafaxine, the HAM-D total score improved by 16.6 +/- 4.9 points. Improvement at 6 weeks was 13.6 +/- 6.3 points for patients treated with imipramine and 10.6 +/- 7.8 points for patients treated with placebo (p < .05 for active drug vs. placebo). Ninety percent of venlafaxine completers were rated as "much" or "very much" improved on the Clinical Global Impression-Improvement scale, compared to 79% treated with imipramine and 53% treated with placebo (p < .05). An endpoint analysis, where the last scores of patients who dropped out were carried forward to subsequent visits, showed significant efficacy only for venlafaxine and not imipramine, probably because of the higher attrition for the latter drug. Overall, both venlafaxine and imipramine were well-tolerated, with venlafaxine having a somewhat lower attrition rate due to adverse effects than imipramine (16% vs. 25%). CONCLUSION: These results, together with those of previously reported studies, suggest that venlafaxine has antidepressant efficacy comparable to that provided by available antidepressants.

Acute Disease↗
PubMed1994

Blood pressure and heart rate response of panic disorder patients receiving imipramine in a dose-response treatment paradigm.

This article reports the effects of imipramine on heart rate and blood pressure in panic disorder patients who participated in an 8-week double-blind dosage response treatment protocol. At the end of a placebo baseline, patients were randomly assigned to placebo or one of three weight-adjusted imipramine dosages: low (0.5 mg/kg per day), medium (1.5 mg/kg per day), or high (3.0 mg/kg per day). It was demonstrated that imipramine had no significant effect on sitting or standing diastolic or systolic blood pressure. Although there was a trend toward a systolic blood pressure drop with positional change, it did not reach statistical significance. There were no significant changes in diastolic blood pressure with postural change. Imipramine did increase sitting and standing heart rate without revealing a clear dosage correlation. In contrast to the pretreated state, the reflex heart rate response to postural change was significantly increased in the posttreatment state, also in a dosage-independent manner. Within the high-dose imipramine group, the baseline sitting to standing heart rate increase was significantly higher in those who dropped out because of drug side effects compared with those who remained. Evidence from this study suggests that imipramine has a dosage-independent effect on resting and reflex heart rate. Future studies should consider postural heart rate reactivity as a potential measure of intolerance to the side effects of high doses of imipramine.

Adult↗
PubMedDate not supplied

Modulation of electroconvulsive treatment induced beta-adrenergic down-regulation by previous chronic imipramine administration: the involvement of protein kinase C.

To test how previous treatment with imipramine affects the action of electroconvulsive shock (ECS) on cortical beta-adrenergic system, male Wistar rats received imipramine, 10 mg/kg b.i.d. for two weeks, followed by 8 days of ECS, and 24 h after the last shock the responsiveness of beta-adrenoceptor system was tested by measuring cyclic AMP formation in cortical slices after exposure to noradrenaline or isoproterenol. To assess the possible role of protein kinase C, the same responses were measured in the presence of a protein kinase C activator, 12-O-tetradecanoyl-phorbol 13-acetate (TPA). ECS alone was found more effective in inducing beta-adrenergic-down-regulation than imipramine, and tended to produce stronger effect when given after chronic imipramine. In contrast to imipramine, which effectively inhibited TPA-induced potentiation of the action of isoproterenol, ECS strongly facilitated it. However, administrated after chronic treatment with imipramine, ECS did not change the potentiation. The results suggest that effects of ECS are slightly modified, but not inhibited by previous administration of imipramine.

Adrenergic beta-Agonists↗
PubMed1997

Economic evaluation of paroxetine and imipramine in depressed outpatients.

In this pilot study, we compared the economic impact of paroxetine and imipramine treatment of depressed outpatients from a university teaching hospital and a community mental health center. A 12-month retrospective chart review of patients was performed. Clinical outcomes including clinic usage, death, relapse, function, adverse effects, psychiatrist visits, and drug costs were evaluated. We analyzed drug costs, psychiatrist costs, and total direct costs using the Mann-Whitney U Test. The incidence of clinic usage, death, function, adverse effects, and psychiatrist visits was similar in patients treated with paroxetine (n = 12) and imipramine (n = 13). Two patients in the imipramine group were hospitalized once for a total of 5 days compared with none in the paroxetine group. Paroxetine drug costs were significantly higher than imipramine drug costs. Direct total costs (i.e., drug, psychiatrist visits, blood levels, and hospitalization costs) did not differ significantly between the groups based on actual drug usage (paroxetine: median $1,432.50 per patient per year; imipramine: median $1,425.81 per patient per year). Although the median direct total cost per patient per year for patients who received 12 months of therapy was lower in the paroxetine group ($1,479.90, n = 8) than the imipramine group ($1,503.61, n = 8), the difference was not significant. Our cost minimization analysis revealed no significant difference in the total cost between the two groups. However, the major cost in the paroxetine group was drug cost, whereas the major cost in the imipramine group was hospitalizations. Future large prospective trials are needed to validate these findings.

Adolescent↗
PubMed1977

Effects of phenobarbital and diazepam on imipramine-induced changes in blood pressure, heart rate and rectal temperature of rats.

To investigate the safety of anticonvulsants in doses found equipotent in suppressing imipramine induced convulsions, the effects of diazepam (1.8 mg/kg) or phenobarbital (40 mg/kg) following a toxic dose of imipramine (50 mg/kg) on heart rate, blood pressure and body temperature were examined in male Wistar rats. Administration of imipramine alone resulted in significant decreases in blood pressure, heart rate and rectal temperature. Phenobarbital or diazepam alone failed to significantly affect any of these parameters apart from a slight reduction in rectal temperature seen with phenobarbital. Diazepam given after imipramine antagonized the imipramine-induced decrease in heart rate but increased the hypotensive and hypothermic effects. Phenobarbital failed to significantly affect the imipramine-induced changes in any of the physiological parameters studied. The present data suggests that phenobarbital may be preferable to diazepam in treatment of imipramine-induced convulsions.

Animals↗
PubMed1987

Regulation of high- and low-affinity [3H]imipramine recognition sites in rat brain by chronic treatment with antidepressants.

Specific binding of [3H]imipramine to its recognition sites in frontal cortex and levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and norepinephrine (NE) as well as uptake of serotonin by crude synaptosomal (P2) fraction were determined in a group of rats chronically (for 21 days) treated with different types of antidepressant drugs: nortriptyline, fluoxetine, iprindole, phenelzine (10 mg/kg per day), maprotiline (20 mg/kg per day) and vehicle only (controls). Quantitative analysis of imipramine competition curves confirmed the existence of two classes of [3H]imipramine sites: high-affinity with IC50 and 11.2 nM and low-affinity with IC50 of 630 nM for the competing ligand. The proportion of high- and low-affinity sites was 73 +/- 4 and 26 +/- 4%, respectively. Chronic treatment with all antidepressant drugs except iprindole significantly decreased the affinity but not the proportion of high-affinity sites for imipramine. IC50 of imipramine at low-affinity sites was even more markedly increased at low-affinity sites by all treatments except for phenelzine. Fluoxetine was by far the most effective in altering the affinity of both high- and low-affinity [3H]imipramine recognition sites. Both NE and 5-HT levels were significantly enhanced only by phenelzine treatment, whereas 5-HT and 5-HIAA levels were found to be lower after fluoxetine. Kinetics of 5-HT uptake were altered significantly only in rats treated with fluoxetine: rate of 5-HT uptake (Vmax) was decreased by 43% and Km value increased from 104 to 184 nM. Changes in affinity of imipramine for its binding sites were not found to be associated with the effect of tested drugs on 5-HT levels or uptake. They may be due to adaptive alterations in physico-chemical properties of binding proteins although the presence of residual drug interfering with the binding assay cannot be excluded. The observed changes are likely to represent the condition during chronic administration of these drugs in clinical therapy of depression.

Animals↗
PubMed1986

Electroconvulsive shock therapy and maximum binding of platelet tritiated imipramine binding in depression.

We studied the tritiated imipramine binding values in platelets from 12 hospitalized untreated patients with endogenous depression and found a significant decrease in maximum binding (Bmax) values compared with a control population of the same age and sex. There were no changes in the equilibrium dissociation affinity constant values between the untreated depressives and the control population. After at least six sessions of electroconvulsive therapy and at the time when a significant clinical improvement of depression was confirmed, the Bmax value of tritiated imipramine binding in platelets was slightly increased but was still significantly below that of the control values. However, when six of these patients were reexamined after 12 to 18 months, at a time when they were euthymic, the Bmax of tritiated imipramine binding in platelets was found in the same range as the values of the control population. Our results indicate that clinical improvement precedes the changes in Bmax of tritiated imipramine binding in platelets from depressed patients. The tritiated imipramine binding in platelets is a useful biologic marker in affective disorders. Furthermore, our results suggest that tritiated imipramine binding in platelets may be a state-dependent biologic marker in depression.

Aged↗
PubMed1987

Imipramine in prepubertal major depressive disorders.

The potential effectiveness of imipramine hydrochloride (up to 5 mg/kg/d) was investigated in 53 prepubertal children suffering from major depressive disorder. Two complementary strategies were used simultaneously: a five-week, double-blind, placebo-controlled design (N = 38), and a plasma level/clinical response study (N = 30). Fifteen of the 16 children randomly assigned to active drug in the first study also participated in the second. Subjects were assessed using the Schedule for Affective Disorders and Schizophrenia for School Age Children and diagnosed according to unmodified Research Diagnostic Criteria. Response rates in the double-blind study were similar in both groups (imipramine, 56%; placebo, 68%). In the plasma level study, total maintenance plasma level (imipramine plus desipramine) was found to positively and linearly predict clinical response of the depressive syndrome (P less than .003). No evidence of a curvilinear relationship was found. Depressive hallucinations during the episode negatively predicted clinical response (P less than .05). Weight-corrected imipramine dosage did not predict either clinical response or plasma level in the individual subject. No predictors of response were found in the placebo group. These results suggest that the mean imipramine dosage was too low, and that future double-blind, placebo-controlled studies of imipramine in prepubertal major depression should include plasma level titration to above 150 ng/mL and an initial placebo washout period.

Age Factors↗
PubMed1988

Marked reduction in the number of platelet-tritiated imipramine binding sites in geriatric depression.

The number (Bmax) and affinity (Kd) of platelet-tritiated imipramine binding sites was determined in young and middle-aged controls 50 years of age and younger (n = 25), elderly normal controls over 60 years of age (n = 18), patients who fulfilled DSM-III criteria for major depression who were under 50 years of age (n = 29), patients who fulfilled DSM-III criteria for major depression who were 60 years of age and older (n = 19), and patients who fulfilled both DSM-III criteria for primary degenerative dementia and National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for probable Alzheimer's disease (n = 13). Both groups of depressed patients (under 50 and over 60 years of age) exhibited significant reductions (decreases 42%) in the number of platelet-tritiated imipramine binding sites with no change in affinity, when compared with their age-matched controls. There was little overlap in Bmax values between the elderly depressed patients and their controls. The patients with probable Alzheimer's disease showed no alteration in platelet-tritiated imipramine binding. There was no statistically significant relationship between postdexamethasone plasma cortisol concentrations and tritiated imipramine binding. These results indicate that platelet-tritiated imipramine binding may have potential utility as a diagnostic adjunct in geriatric depression, and moreover that the reduction in the number of platelet-tritiated imipramine binding sites is not due to hypercortisolemia.

Adolescent↗
PubMed1998

Imipramine treatment of opiate-dependent patients with depressive disorders. A placebo-controlled trial.

BACKGROUND: The literature is inconclusive on the role of antidepressant medications in treating drug dependence. Studies have either not focused on depressed patients or have selected patients with depressive disorders based on cross-sectional symptoms rather than a syndromal diagnosis. A clinical trial of an antidepressant was, therefore, conducted on drug-dependent patients with syndromal depression. METHODS: Patients receiving methadone hydrochloride maintenance treatment were selected if they met the criteria for a DSM-III-R depressive disorder that was chronologically primary, had persisted during a past abstinent period or was long-standing, and persisted during at least 1 month of stable methadone treatment. Subjects were randomized to a 12-week, double-blind, placebo-controlled trial of imipramine hydrochloride. A favorable response was defined as a Clinical Global Impression scale score for depression of 2 ("much improved") or 1 ("very much improved") and at least a 75% reduction in self-reported drug or alcohol use or abstinence. RESULTS: One hundred thirty-seven patients were randomized, and 84 completed a minimum adequate trial of at least 6 weeks. Among the 84 adequately treated patients, 57% (24/42) receiving imipramine were rated as responders compared with 7% (3/42) receiving placebo (P < .001). On measures of mood, there was a robust effect of imipramine. Imipramine was superior to placebo on some self-reported measures of substance use and craving, and mood improvement was associated with improvement in self-reported substance use. However, few patients achieved urine-confirmed abstinence. CONCLUSIONS: Imipramine was an effective antidepressant in patients receiving methadone who were selected via syndromal criteria for depressive illness. Imipramine may reduce substance abuse among patients whose mood improves; however, this effect was less robust.

Adult↗
PubMed2002

Double-blind switch study of imipramine or sertraline treatment of antidepressant-resistant chronic depression.

BACKGROUND: Although various strategies have been proposed to treat antidepressant nonresponders, little controlled research has been published that examines prospectively the use of switching to an alternate antidepressant. METHODS: This was a multisite study in which outpatients with chronic major depression (with or without concurrent dysthymia), who failed to respond to 12 weeks of double-blind treatment with either sertraline hydrochloride (n = 117) or imipramine hydrochloride (n = 51), were crossed over or switched to 12 additional weeks of double-blind treatment with the alternate medication. Outcome measures included the 24-item Hamilton Rating Scale for Depression and the Clinical Global Impressions--Severity and Improvement scales. RESULTS: The switch from sertraline to imipramine (mean dosage, 221 mg/d) and from imipramine to sertraline (mean dosage, 163 mg/d) resulted in clinically and statistically significant improvements. The switch to sertraline treatment was associated with fewer adverse effect complaints and significantly less attrition owing to adverse effects. Although sertraline treatment also resulted in significantly higher response rates in the intent-to-treat samples (60% in the sertraline group and 44% in the imipramine group), neither the intent-to-treat remission rates nor the response and remission rates among study completers differed significantly. Moreover, after considering the effect of attrition, there were no significant treatment effects on the more comprehensive generalized estimating equation analyses of the continuous dependent measures. CONCLUSIONS: More than 50% of chronically depressed antidepressant nonresponders benefited from a switch from imipramine to sertraline, or vice versa, despite a high degree of chronicity. As in the initial trial, sertraline was generally better tolerated than imipramine. Switching to a standard antidepressant of a different class is a useful treatment strategy for antidepressant nonresponders and could be considered a standard of comparison for future studies of novel alternate strategies.

Adult↗
PubMed1996

Trimipramine and imipramine exert different effects on the sleep EEG and on nocturnal hormone secretion during treatment of major depression.

In a 4-week double-blind clinical trial we compared the effects of the tricyclic antidepressants trimipramine and imipramine on the sleep EEG and on nocturnal bormone secretion in 20 male inpatients with major depression. Both treatments produced rapid significant clinical improvement in depression without severe adverse effects. However, the two drugs had markedly different neurobiologic profiles. Trimipramine enhanced rapid eye movement (REM) sleep and slow wave sleep, whereas imipramine suppressed REM sleep and showed no effect on slow wave sleep. Total sleep time and the sleep efficiency index increased under trimipramine but not under imipramine. Nocturnal cortisol secretion decreased with trimipramine but remained unchanged with imipramine. In contrast to imipramine, trimipramine induced an increase in prolactin secretion compatible with its known antagonism at dopamine (D2) receptors. Imipramine induced a decrease in growth hormone secretion during the first half of the night. Neither of the drugs induced significant changes in plasma testosterone concentration. We conclude that trimipramine is an antidepressant with sleep-improving qualities that possibly acts through inhibition of hypothalamic-pituitary-adrenocortical system activity by a yet unknown mechanism.

Adult↗
PubMed2001

Effect of concurrent anxiety on response to sertraline and imipramine in patients with chronic depression.

Anxiety commonly complicates the clinical presentation of depression and has been associated with poorer long-term outcome, but little information is available on the clinical correlates, and comparative effect on treatment response, of subsyndromic or secondary anxiety. Patients diagnosed with chronic major or double depression were randomized to 12 weeks of double-blind treatment with either sertraline or imipramine in a 2:1 ratio. A high anxiety subgroup was operationally defined by a HAM-D anxiety/somatization factor score > or = 7. The effect of study treatment was measured utilizing the HAM-D, CGI, HAM-D anxiety/somatization factor, as well as a quality of life measure (Q-LES-Q) and a measure of psychosocial functioning (the MOS-SF-36). Two hundred nine patients were treated with imipramine and 426 patients were treated with sertraline. Thirty-six percent of the total met criteria for the high anxiety subgroup. According to Kaplan-Meier probability estimates, patients with significant concurrent anxiety symptoms were more likely to respond by 12 weeks (66.4%) than those without significant anxiety symptoms (54.2%). There was no significant difference in response rates for sertraline vs. imipramine. Both drugs were effective at treating high baseline levels of anxiety, with 60% of sertraline patients and 58% of imipramine patients having 50% or greater reduction from baseline in HAM-D anxiety/somatization factor scores, and only 4.6% and 9.9%, respectively, reporting treatment-emergent worsening in anxiety at study endpoint. Despite the chronicity of depressive illness, acute treatment with both sertraline and imipramine significantly improved psychosocial and quality of life measures. High baseline levels of anxiety did not reduce overall antidepressant response but did somewhat delay the onset of response to sertraline or imipramine in patients with chronic depression.

Adrenergic Uptake Inhibitors↗
PubMed1994

Lactate-induced anxiety after imipramine and diazepam treatment.

To examine the effect of treatment on lactate-induced anxiety in a controlled study, we infused 44 panic disorder patients with lactate and placebo before and after eight weeks of double-blind treatment with imipramine, diazepam, or placebo. During treatment, both imipramine and diazepam groups improved more than the placebo group. After treatment, patients in both the imipramine and diazepam groups had significantly less anxiety than the placebo patients when reinfused with lactate. In addition, imipramine decreased posttreatment panic attack frequency and diazepam decreased the perceived severity of posttreatment lactate-induced panic attacks. This study demonstrates that diazepam, like imipramine, is an effective treatment for panic disorder, and that both imipramine and diazepam blunt lactate-induced anxiety in a placebo controlled study.

Adolescent↗
PubMed1978

Determination of imipramine in plasma by high pressure liquid chromatography and field ionization mass spectrometry: increased sensitivity in comparison with gas chromatography mass spectrometry.

A quantitative method is reported for the determination of imipramine in plasma samples in the low nanogram and subnanogram range. The sensitivity and precision of the technique, which involves high pressure liquid chromatography and direct probe field ionization mass spectrometry, are approximately an order of magnitude greater than are offered by gas chromatography mass spectrometry with selected ion monitoring using deuterated or other types of internal standards. [2H6]Imipramine, labeled in the ethylene bridge and in the aromatic rings, serves as the isotopic diluent. The method has been used for the determination of the comparative bioavailabilities of two different commercial preparations of imipramine. In these tests, subjects ingested a 25 mg tablet of one or the other drug preparation together with a solution containing an equivalent amount of imipramine deuterated in the ethylene bridge ([2H2]imipramine). The latter served as an internal check for intrasubject variability in absorption of the imipramine tablets. Typical results from one of the subjects are presented.

Adolescent↗
PubMed1986

Chronic antidepressant treatment and mouse brain 3H-imipramine binding.

Chronic pretreatment of mice with the monoamine oxidase type B inhibitor (-)deprenyl resulted in an increase in the density of cerebral cortical 3H-imipramine binding sites and a decrease in the density of cerebral cortical beta-adrenergic receptors. In contrast, pretreatment of mice with the tricyclic antidepressants imipramine and desipramine did not alter the density of cerebral cortical 3H-imipramine binding sites. Imipramine and desipramine treatment decreased the density of beta-adrenergic receptors. Haloperidol pretreatment resulted in an increase in the density of striatal D-2 dopamine receptors, but did not alter the density of cerebral cortical 3H-imipramine binding sites or beta-adrenergic receptors. These data suggest that brain 3H-imipramine binding sites can be regulated by pharmacological pretreatment, but that this regulation may not occur for all antidepressants.

Animals↗
PubMed1977

Alterations induced in distribution and in vivo metabolism of imipramine by pregnenolone-16alpha-carbonitrile.

Female rats were given pregnenolone-16alpha-carbonitrile (I) to investigate its in vivo effects on the loss of the righting reflex and the mortality rate induced by imipramine as well as the concentrations of this drug and its metabolite, desipramine, in plasma, brain, liver, lungs, and kidneys. The protective action of I was associated with diminished organ levels of imipramine (catatoxic mechanism), and the relationship between brain and plasma imipramine concentrations remained unaltered. Desipramine-imipramine molar ratios were increased, indicating an elevated rate of N-demethylation. The unbound imipramine in plasma was diminished, but the relationship between protein-bound and unbound imipramine levels was not modified.

Animals↗
PubMed2005

Modafinil enhances the increase of extracellular serotonin levels induced by the antidepressant drugs fluoxetine and imipramine: a dual probe microdialysis study in awake rat.

In view of a postulated role of the vigilance-promoting drug modafinil in depression, the interaction of modafinil and two classical antidepressant drugs, fluoxetine and imipramine, were studied in 5-HT levels in the dorsal raphe-cortical system using dual-probe microdialysis. Fluoxetine (1-10 mg/kg) dose-dependently increased dorsal raphe-cortical 5-HT levels. Modafinil at a very low dose (3 mg/kg), by itself ineffective, enhanced the fluoxetine (5 mg/kg)-induced increases of 5-HT levels in both brain areas. A synergistic interaction was observed in the prefrontal cortex with fluoxetine (1 mg/kg) in terms of 5-HT release, but not in the dorsal raphe. Imipramine (1.3 mg/kg) increased 5-HT levels in the dorsal raphe, but not in the prefrontal cortex, while the higher doses (10.9-21.8 mg/kg) caused substantial increases in both brain areas. Modafinil (3 mg/kg), injected before imipramine (1.3 mg/kg), which by itself was ineffective on cortical 5-HT levels, increased cortical 5-HT levels. On other hand, modafinil failed to affect the high-dose imipramine (10.9 mg/kg)-induced increase of 5-HT levels in the prefrontal cortex and the imipramine (1.3; 10.9 mg/kg)-induced increase of 5-HT levels in the dorsal raphe nucleus. These results demonstrate that modafinil in low doses enhances the acute effects of fluoxetine and imipramine on 5-HT levels in the dorsal raphe nucleus (fluoxetine only) and especially in the prefrontal cortex of the awake rat. These findings suggest a therapeutic potential of low doses of modafinil in the treatment of depression when combined with low doses of classical antidepressants, especially by increasing 5-HT transmission in cortical regions.

Animals↗