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PubMed1990

Efficacy of a reversible monoamine oxidase-A inhibitor versus imipramine in subgroups of depressed patients.

Two multicentre studies comparing moclobemide with imipramine under similar conditions in patients undergoing a major depressive episode (DSM-III) were combined in the present analysis. A total of 353 patients received moclobemide (300-600 mg/day) and 356 imipramine (100-200 mg/day). In each study, the antidepressant efficacy of the 2 drugs was comparable, and subgroup analysis showed that moclobemide and imipramine were equally effective in endogenous depression. The response rate did not appear to be influenced by sex, but patients older than 60 years tended to respond less well to both drugs than did those under 60. The conclusion from the 2 studies is that, contrary to what is frequently stated for monoamine oxidase inhibitors, moclobemide appears as effective as a tricyclic in treating endogenous depression.

Antidepressive Agents↗
PubMed1991

Paroxetine and imipramine treatment of depressive patients in a controlled multicentre study with plasma amino acid measurements.

In a 12-week double-blind study with 36 patients with major depressive episode (DSM-III), paroxetine (Seroxat, Aropax) showed significantly quicker onset of efficacy on the Melancholia Scale, and better tolerance than imipramine. Plasma concentration analyses showed no clear concentration-efficacy correlation in either treatment group. During long-term treatment paroxetine seemed to be superior to imipramine in preventing relapse; both treatments were well tolerated. A significant correlation between baseline plasma tryptophan: large neutral amino acids ratio and final Hamilton Rating Scale for Depression (HRSD) score and a trend towards an inverse correlation between this ratio and percentage reduction in HRSD score were seen in the paroxetine group but not in the imipramine group. In line with previous studies, these results support the hypothesis that paroxetine is an effective and well tolerated antidepressant.

Amino Acids↗
PubMed1992

Paroxetine and imipramine in the treatment of depressive patients in psychiatric practice.

A total of 151 outpatients with endogenous or mixed endogenous and reactive depression were included in a 6-week double-blind study, with extension for up to 1 year, in psychiatric practice. The results showed trends in efficacy variables and a statistically significant difference in a benefit-risk ratio in favour of paroxetine (Seroxat, Paxil) compared with imipramine. Efficacy was largely maintained in both groups during long-term treatment. The frequency and severity of side effects in paroxetine patients declined markedly from short-term to long-term treatment, whereas changes in imipramine patients were less pronounced. Significantly more imipramine patients gained weight during long-term treatment. In conclusion, paroxetine is an effective and well tolerated antidepressant, well suited for outpatients in psychiatric practice.

Adolescent↗
PubMed1993

A comparison of fluoxetine and imipramine in the treatment of outpatients with major depressive disorder.

A double-blind clinical trial was undertaken to evaluate the clinical efficacy and safety of fluoxetine compared with imipramine in the treatment of 59 outpatients suffering from major depressive disorder. The mean scores of all depression rating scales showed that the drugs had comparable efficacy. The side effect profile of imipramine was found to be mainly anticholinergic, which was not the case for fluoxetine, where it was mainly found to be gastrointestinal, such as nausea and diarrhoea. In both groups the total number of adverse events reported were the same. Fluoxetine treatment resulted in weight loss, whereas imipramine treatment resulted in a slight but significant weight increase.

Adolescent↗
PubMed1980

Imipramine cardiotoxicity: an electrocardiographic and haemodynamic study in rabbits.

The purpose of the present study was to investigate the cardiotoxicity of the tricyclic antidepressant imipramine. The experiments were carried out in rabbits during continous intravenous infusion of imipramine, and electrocardiographic and haemodynamic changes were observed. The blood flows were measured using the radioactive microsphere method based upon the principles of Fick and Stewart Hamilton. It was found that the decrease in heart rate and the changes in heart rhythm were always preceded by a fall in arterial blood pressure and cardiac contractility, expressed by a fall in dp/dtmax. On the basis of the results it is concluded that a direct depressing action on the myocardium is of importance in the development of cardiac complications, although both a depressing influence on cardiac conduction, an anticholinergic effect, and an influence on adrenergic factors may also contribute. The possibility of positive correlations between the changes in plasma-imipramine concentration and the changes in the dp/dtmax and the QRS complex cannot be excluded.

Animals↗
PubMed1986

Cortical beta- and alpha 2- adrenoceptor binding, hypothalamic noradrenaline and pineal melatonin concentrations measured at different times of the day after repeated treatment of rats with imipramine, zimeldine, alaproclate and amiflamine.

The effect of repeated treatment of rats for 21 days with the monoamine reuptake inhibitors imipramine, zimeldine, alaproclate (in each case 10 mumol/kg b.i.d.) and the reversible monoamine oxidase-A inhibitor amiflamine (3 mumol/kg b.i.d.) on brain noradrenergic mechanisms measured at different times of the day and night was investigated. Imipramine treatment produced a down-regulation of the Bmax for 3H-dihydroalprenolol binding to cortical beta-adrenoceptors that was not dependent upon the time of day the animals were killed. Zimeldine, on the other hand, reduced both Bmax and Kd of binding for day-time, but not night-time samples. Alaproclate and amiflamine were without effect on the binding. Twenty-four hour mean values for 1 nM 3H-p-aminoclonidine binding to alpha 2-adrenoceptors were lower for the zimeldine-treated rats than for the saline-treated rats. Pineal melatonin concentrations, which are regulated by beta-adrenoceptors, showed a pronounced diurnal rhythm, with the highest concentrations being found at 02:00. At this time point, a lower pineal melatonin content was found after amiflamine treatment, whereas imipramine, zimeldine and alaproclate were without significant effect. The importance of the use of more than one time point and the use of more than one biochemical test for the determination of the effects of repeated antidepressant treatment on central noradrenergic systems measured ex vivo is discussed.

Alanine↗
PubMed2002

Inhibition of Na(+) current by imipramine and related compounds: different binding kinetics as an inactivation stabilizer and as an open channel blocker.

Use-dependent block of Na(+) channels plays an important role in the action of many medications, including the anticonvulsants phenytoin, carbamazepine, and lamotrigine. These anticonvulsants all slowly yet selectively bind to a common receptor site in inactivated but not resting Na(+) channels, constituting the molecular basis of the use-dependent block. However, it remains unclear what channel gating process "makes" the receptor, where the receptor is located, and how the slow drug binding rate (to the inactivated channels) is contrived. Imipramine has a diphenyl structural motif almost identical to that in carbamazepine (a dibenzazepine tricyclic compound), as well as a tertiary amine chain similar to that in many prototypical local anesthetics, and has also been reported to inhibit Na(+) channels in a use-dependent fashion. We found that imipramine selectively binds to the inactivated (dissociation constant approximately 1.3 microM) rather than the resting Na(+) channels (dissociation constant >130 microM). Moreover, imipramine rapidly blocks open Na(+) channels, with a binding rate approximately 70-fold faster than its binding to the inactivated channels. Similarly, carbamazepine and diphenhydramine are open Na(+) channel blockers with faster binding rates to the open than to the inactivated channels. These findings indicate that the anticonvulsant receptor responsible for the use-dependent block of Na(+) channels is located in or near the pore (most likely in the pore mouth) and is made suitable for drug binding during channel activation. The receptor, however, continually changes its conformation in the subsequent gating process, causing the slower drug binding rates to the inactivated Na(+) channels.

Adrenergic Uptake Inhibitors↗
PubMed1970

Norepinephrine turnover and metabolism in rat brain after long-term administration of imipramine.

The rate of disappearance of intracisternally administered tritiated norepinephrine from rat brain is decreased after a single dose of the tricyclic antidepressant imipramine. During long-term administration of imipramine, however, the rate of disappearance of tritiated norepinephrine from brain gradually increases, and there is a concurrent decrease in the content of endogenous norepinephrine in brain. These findings may help to explain why antidepressant effects are observed clinically only after long-termn treatment with imipramine.

Animals↗
PubMed1981

Imipramine: effect of ovarian steroids on modifications in serotonin receptor binding.

Long-term administration of imipramine caused a decrease in serotonin2 receptor binding in rat brain cerebral cortex, an effect that was abolished by ovariectomy. In contrast, ovariectomy had no effect on imipramine-induced decreases in hippocampal serotonin or in cerebral cortical and hippocampal beta-adrenergic receptor binding. Administration of estradiol or progesterone separately or in combination reestablished the effect of imipramine treatment on cortical serotonin2 receptors. These results suggest that ovarian steroids may play an important, but subtle, role in the neurochemical and perhaps clinical response to this drug.

Animals↗
PubMed1980

High-affinity [3H]imipramine binding in rat hypothalamus: association with uptake of serotonin but not of norepinephrine.

Inhibition of the binding of [3H]imipramine and inhibition of the uptake of [3H]serotonin and [3H]norepinephrine by a series of antidepressants and other drugs were studied in the rat hypothalamus. No correlation was found between the potencies of these drugs for the inhibition of [3H]imipramine binding and the inhibition of [3H]norepinephrine uptake. There was, however, a highly significant correlation between the potencies of these drugs for the inhibition of [3H]serotonin uptake. These results suggest that high-affinity [3H]imipramine binding might be associated with the mechanism of serotonin uptake in the brain.

Animals↗
PubMed1984

Influence of embolism and imipramine on kinetics of serotonin uptake by dog lung.

We previously presented a model from which the kinetic parameters Km and Vmax for serotonin uptake by the lung can be obtained from multiple indicator-dilution data. The purpose of the present study was to determine whether experimentally induced changes in lung endothelial function would be revealed in the kinetic parameters calculated using the model. In experiments using isolated dog lung lobes, embolization with 550-microns glass beads was used to reduce the vascular volume and perfused surface area. Imipramine was used to inhibit the serotonin uptake mechanism. In addition, we studied the influence of the vasodilator papaverine, which in previous studies had been used to block the serotonin-induced vasoconstriction. Embolization, imipramine, and papaverine all significantly reduced percentage uptake of serotonin. The kinetic analysis revealed a significant decrease in the maximum serotonin uptake rate (Vmax) with all three experimental manipulations. In addition, imipramine significantly increased Km. The results indicate that the kinetic parameters obtained from the model do respond to transport inhibition and changes in endothelial surface area, further supporting their usefulness as indexes of endothelial function.

Animals↗
PubMed2000

Combination therapy of imipramine with oxybutynin in children with enuresis nocturna.

PURPOSE: The treatment approach for enuresis is controversial due to the lack of consensus as to the exact causes of nocturnal enuresis. Despite various treatment modalities, pharmacotherapy still appears to be the common choice. The aim of this prospective study was the evaluation of the efficacy of combination therapy (imipramine and oxybutynin) in patients with enuresis nocturna. PATIENTS AND METHODS: This prospective study was done with 77 monosymptomatic nocturnal enuretics between July 1996 and December 1998. RESULTS: Even though there is no statistically significant difference between combination therapy (imipramine plus oxybutynin) and monotherapy, clinical data showed that combination therapy is more effective. CONCLUSIONS: We conclude that combination of imipramine with oxybutynin is a safe and new choice in the treatment of nocturnal enuresis.

Adolescent↗
PubMed1986

Preliminary clinical experience with imipramine HCl in the treatment of sleep apnea syndrome.

In the last 2 years we have systematically treated 31 sleep apnea patients with 25-50 mg imipramine HCl given 30 min before bedtime. Imipramine treatment was attempted for nonoverweight patients with negative ear, nose and throat (ENT) findings and for patients who had not responded to weight reduction or ENT surgery (in all patients the apneas were not considered life threatening). Thirteen of the 31 (41.9%) patients, of whom 9 had central apnea, reported subjective improvement in diurnal and nocturnal symptoms within 10-15 days from the initiation of treatment. Sleep laboratory recordings conducted 1-5 months after the beginning of treatment revealed a significant decrease in the total number of apneas from 242 +/- 156 to 142.8 +/- 120.1 (p less than 0.01) in these patients. We concluded that treatment with imipramine may benefit selected sleep apnea patients particularly of the central type.

Adult↗
PubMed1979

Prediction of antidepressant responses to imipramine.

45 patients hospitalized for depression who had received double-blind trials with imipramine were examined for possible associations between pretreatment responses to the Minnesota Multiphasic Personality Inventory (MMPI) and their behaviorally-rated responses to this drug. Each patient was randomly assigned to one of two groups with the restriction that the number of responders and nonresponders be balanced for sex. Results from the group A patients suggest that responders and nonresponders to imipramine were best identified by using two sex-specific, empirically-derived, MMPI scales. In contrast, 12 of 13 regular validity and clinical scales and all 49 of the selected special scales of the MMPI failed to separate responders from nonresponders. In the cross-validation study with the group B patients, we were able to predict female and male responders from nonresponders by the new imipramine response scale with accuracy rates of 93 and 100%, respectively. The implications of these results are discussed.

Depression↗
PubMed1987

Platelet 3H-imipramine binding and familial transmission of affective disorders.

We studied platelet 3H-imipramine binding and family history of affective illness in 26 patients with bipolar affective disorder and 24 patients with unipolar affective disorder. The density of platelet 3H-imipramine binding sites (Bmax) was significantly lower in bipolar patients with family history of affective illness than in healthy controls; however, there was a considerable overlap in Bmax values between the familial cases and the normal controls. A similar trend was observed in familial cases of unipolar disorder but the differences fell short of statistical significance. The nonfamilial cases of affective disorder did not differ from the healthy controls. The possible role of reduced platelet 3H-imipramine binding as a genetic vulnerability 'marker' in affective disorder was discussed.

Adult↗
PubMed1989

Long-term effects of alprazolam and imipramine on cerebrospinal fluid monoamine metabolites and neuropeptides in panic disorder.

Cerebrospinal fluid (CSF) homovanillic acid, 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxyphenylglycol, and somatostatin and beta-endorphin levels were measured in 12 patients with panic disorder before and after 7 months of treatment with alprazolam or imipramine. The concentrations of CSF monoamine metabolites and neuropeptides were at baseline of the same order of magnitude in panic patients and controls. Neither alprazolam nor imipramine changed metabolite or neuropeptide levels in CSF despite clinical improvement in both treatment groups. According to present CSF data, the antipanic actions of alprazolam and imipramine do not involve the monoaminergic or peptidergic systems studied.

Adult↗
PubMed1992

Effect of imipramine treatment on heart rate variability measures.

Recently, heart rate (HR) variability has received considerable attention, and a decreased HR variability has been linked to a significant risk of cardiovascular illness. We have previously reported such a decreased variability in panic disorder patients. In this study, we report on HR variability in 12 depressed and 6 panic disorder patients at baseline and 1 and 3 weeks of treatment with imipramine as measured by the standard deviation, mean consecutive difference and the standard deviation of the mean consecutive difference of the R-R intervals in supine, supine deep breathing and standing postures. In all subjects, imipramine (mean dose: 70 mg/day) produced a significant decrease in heart rate variability at week 3 as measured by the above variables. This decrease in HR variability during imipramine treatment is probably due to its anticholinergic effects.

Adult↗
PubMed1976

Role of brain monoamines in the anticonvulsant effect of imipramine in albino rats.

The role of brain monoamines in the anticonvulsant effect of imipramine was investigated in albino rats, against maximal electroshock-induced seizures, by using drugs with well-defined effects on brain monoamines. The results suggest a definite role for noradrenaline in imipramine anticonvulsant action. Dopamine and 5-hydroxytryptamine do not appear to be involved in this effect of imipramine.

Animals↗