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PubMed1979

Imipramine affects autonomic control of sinoatrial rate in isolated right atrial preparations.

The effects of imipramine on sinoatrial rate and chronotropic responses to transmural stimulation (TS) were studied in the isolated guinea-pig right atrial preparation. The negative chronotropic response (cholinergically mediated rate decrease) to TS was progressively inhibited by imipramine (5 x 10(-6) M). This inhibition can be attributed directly to an "atropine-like" effect of this drug. The positive chronotropic response (adrenergically mediated rate increase) to TS was markedly potentiated by imipramine at similar therapeutic doses; higher doses (5 x 10(-5) M) substantially depressed this rate response. This depression of the adrenergic response to TS does not appear to be the result of a blockade of beta adrenergic receptors since imipramine still potentiated the rate increase in response to exogenous norepinephrine at doses where no TS response remained. Basal spontaneous rate was also depressed by imipramine at high doses (5 x 10(-5) M), both in the absence and presence of autonomic blockers.

Acetylcholine↗
PubMed1982

Controlled trial of imipramine for chronic low back pain.

Chronic low back pain is a common problem that has been noted in several studies to exist as a component of masked depression. To determine the usefulness of imipramine in the treatment of chronic low back pain, either by a direct action or indirectly via resolution of a depressive equivalent, 50 consecutive patients were entered into a controlled trail that employed serum imipramine and desipramine levels and Beck depression questionnaires. Forty-one patients completed the study, and 48 were used in the statistical analysis. Imipramine had a statistically significant effect over placebo in most, but not all, of the clinical parameters that were measured. A linear relationship between serum drug levels and reported symptoms was not noted. Only 10 of the 50 patients entered into the study were judged clinically depressed and, of these, 7 were depressed according to standard criteria. There was no statistically significant difference noted in either the initial or the change in Beck depression scores between those on imipramine and those on placebo. However, among those on the active drug, the patients with a greater symptomatic response had a simultaneous change in the total Beck depression scores (toward less depression) that approached statistical significance when compared with those with a less symptomatic response. Although the results are not conclusive, imipramine may possibly be useful in the treatment of chronic low back pain, especially so when it exists as a component of masked depression.

Adult↗
PubMed1983

(3H)-imipramine binding and plasmid replication sites in Escherichia coli.

Binding of (3H)-imipramine to F'lac plasmid-carrying E.coli was studied. The binding was saturated at 500 mM imipramine in the case of F'lac cells, and the imipramine binding of plasmid-carrying bacteria was inhibited by several tricyclic compounds, such as acridine orange, desimpramine and promethazine. Methylene blue enhanced the (3H)-imipramine binding of bacteria. Binding of radioactively labelled pBR322 plasmid DNA to the internal membrane was more efficient in the presence of plasmid-eliminating drugs than in that of their ineffective derivatives. It is concluded that a structural association exists between imipramine binding and plasmid replication sites in bacteria. The plasmid DNA is assumed to bind irreversibly to its replication site in the presence of the drug and this process can lead to plasmid elimination.

Antidepressive Agents, Tricyclic↗
PubMed1984

Imipramine treatment of painful diabetic neuropathy.

Twelve patients with severe, painful diabetic neuropathy in the lower extremities were treated with imipramine and placebo in a fixed-dose, double-blind, crossover study of five plus five weeks. Seven patients experienced notable improvement while receiving imipramine and none while receiving placebo. The rating of specific symptoms at the end of each treatment period showed a beneficial effect of imipramine on pain, paresthesia, dysesthesia, numbness, and nocturnal aggravation. The plasma levels of imipramine and its metabolite desipramine were significantly higher in patients who benefited from imipramine treatment.

Adult↗
PubMed1984

A double-blind comparative evaluation of the efficacy and safety of nomifensine, imipramine, and placebo in depressed geriatric outpatients.

Nomifensine, imipramine, and placebo were compared in 61 depressed geriatric outpatients over a 35-day period. At average daily doses of 150 mg, nomifensine and imipramine were significantly more effective than placebo in reducing symptoms of depression in this sample of elderly depressed patients. Nomifensine and imipramine were generally comparable in clinical effect; 78% of the nomifensine-treated patients were rated as improved at the end of treatment as compared with 64% of imipramine and 20% of placebo patients. The findings suggest a more favorable side effect profile for nomifensine, which was associated with a lower frequency of sedating and anticholinergic effects than was seen in the imipramine group.

Aged↗
PubMed1984

Fluoxetine in depressed patients: a comparison with imipramine.

The clinical efficacy and safety of fluoxetine and imipramine were compared in a double-blind, 5-week, parallel study in 40 depressed outpatients. Mean scores for most depression scales improved more in patients taking fluoxetine than in those receiving imipramine (p less than .05). Nine of 16 (56%) fluoxetine patients who completed the study and 1 of 19 (5%) imipramine patients were not at all depressed at the end of the study (p less than .001). Seven fluoxetine patients and 14 imipramine patients reported one or more adverse effects during treatment; no fluoxetine patient terminated the study early for drug-related reasons. It was concluded that fluoxetine provides effective antidepressant activity with fewer and less troublesome side effects than imipramine.

Adult↗
PubMed1983

Clinical pharmacology of bupropion and imipramine in elderly depressives.

The clinical efficacy and adverse reaction profile of bupropion, an atypical antidepressant, was compared with the tricyclic imipramine in 63 elderly depressives. Patients were randomly assigned to treatment with 150 or 450 mg/day of bupropion, 150 mg/day of imipramine, or placebo for 35 days. Both doses of bupropion were equivalent to imipramine in antidepressant efficacy. The higher dose of bupropion had a more rapid onset of effect than the low dose and significantly greater anxiolytic activity than either imipramine or the lower dose. Both doses of bupropion had adverse reaction profiles strikingly similar to placebo and, in marked contrast to imipramine, did not produce sedation or anticholinergic side effects. Cognition improved equally in all groups. It was concluded that bupropion has therapeutic advantages over the tricyclics in the treatment of elderly depressives.

Age Factors↗
PubMed1984

Concentrations of imipramine and its metabolites during enuresis therapy.

Plasma concentrations of imipramine and three of its metabolites were determined in children 6 to 15 years of age who received imipramine for treatment of nocturnal enuresis. In 14 patients with reliable data the reduction in wet nights after beginning drug therapy had no apparent relationship to either imipramine concentration alone or imipramine combined with its metabolites. This finding may be related to the relatively low drug concentrations in this group of patients, a high placebo response rate, or noncompliance with the prescribed dosage regimen. Determining plasma imipramine concentrations during treatment for enuresis has questionable value as an aid to improve clinical response. This practice may occasionally be justified when avoidance of toxicity is a major concern.

Adolescent↗
PubMed1982

Effect of pregnenolone-16 alpha-carbonitrile on the biliary and urinary excretion of imipramine and some of its metabolites in rats.

The influence of pregnenolone-16 alpha-carbonitrile (PCN) upon the biliary and urinary excretion of unchanged imipramine and some of its metabolites was investigated in female rats. The substrate and its metabolites were identified and quantified by thin-layer chromatography and/or gas-liquid chromatography. PCN augmented urinary excretion of desipramine and the imipramine- and desipramine-glucuronides. PCN pretreatment also diminished the urinary elimination of imipramine N-oxide whereas proadifen hydrochloride had an inverse effect, suggesting a shift in the metabolic pathways of imipramine. The biliary excretion of the imipramine and desipramine glucuronides was not significantly altered by PCN.

Animals↗
PubMed1982

Release of creatine kinase and lactate dehydrogenase from frog skeletal muscles treated with imipramine.

Frog sartorius and extensor longus digiti IV ("toe") muscles were mounted in sample collecting units, isometric tension was recorded and the activities of creatine kinase and lactate dehydrogenase released into the bathing medium were measured. Addition of imipramine (greater than 0.2 mM) to the control medium induced muscle contractures and increased the rates of enzyme release. Electronmicrographs of muscles exposed to imipramine (0.5--1.0 mM) showed fibers in which the extracellular marked horseradish peroxidase was detected in the sarcoplasm. Both the enzyme-releasing and the contractile effects of imipramine were inhibited by procaine (but not by lidocaine) and were enhanced by replacement of external chloride ions with propionate. The data are consistent with the suggestion that events associated with tension development contribute greatly to the imipramine-induced loss of sarcoplasmic enzymes from frog skeletal muscles. The elevated Ca++ concentration in the sarcoplasm during the imipramine-induced contracture is thought to lead to changes in the plasma membrane that account for the increased enzyme loss and for the penetration of horseradish peroxidase into the sarcoplasm.

Animals↗
PubMed1981

Effect of imipramine on high potassium evoked 3H-dopamine release in the rat striatum.

The effects of three different types of dopamine (DA) uptake inhibitor, imipramine, cocaine and nomifensine, were examined on high potassium evoked 3H-DA release using tissues obtained from rat striatum by a micropuncture technique. Imipramine caused an increase in 3H-DA efflux and this imipramine-induced efflux is Ca2+-independent. Moreover, imipramine reduced the high potassium evoked release, and at 50 microM, the release by potassium stimulation was entirely abolished. These results support that imipramine depletes vesicular DA which is released by potassium stimulation as well as an inhibitory effect on DA uptake. However, nomifensine dose not have such an effect.

Animals↗
PubMedDate not supplied

Effects of imipramine and amitriptyline on intraventricular conduction, effective refractory period, incidence of ventricular arrhythmias induced by programmed stimulation, and on electrocardiogram after myocardial infarction in dog.

The effects of imipramine and amitriptyline on intraventricular conduction, effective refractory period, incidence of ventricular arrhythmias induced by programmed stimulation and on electrocardiogram changes were studied after myocardial infarction in the dog. Amitriptyline, at doses of 1-3 mg/kg, significantly slowed the ventricular conduction of the infarcted zones in a dose- and frequency-dependent manner. Amitriptyline, at doses of 2 and 3 mg/kg, slowed the ventricular conduction slightly in the normal zone. The effective refractory period was prolonged by amitriptyline at a dose of 1 mg/kg. Amitriptyline increased the incidence of ventricular arrhythmias induced by programmed stimulation. Amitriptyline, at doses of 1-3 mg/kg, increased heart rate and prolonged the PQ, QRS and QT interval. Imipramine, at a dose of 3 mg/kg, slowed the conduction in infarcted zones to a lesser extent than amitriptyline. Imipramine, at doses of 1 and 2 mg/kg, did not significantly increase the incidence of ventricular arrhythmias. Imipramine, at a dose of 3 mg/kg, prolonged the QRS interval. From the present results it appears that imipramine has a lower cardiac toxicity than amitriptyline.

Amitriptyline↗
PubMed1994

Metabolic disposition of imipramine in oriental subjects: relation to metoprolol alpha-hydroxylation and S-mephenytoin 4'-hydroxylation phenotypes.

We studied the metabolic disposition of imipramine by measuring imipramine and its metabolites in plasma and urine simultaneously after a single oral dose of 25 mg of imipramine hydrochloride administered to 16 healthy (three Japanese and 13 Korean) volunteers. Four of the subjects were poor metabolizers (PMs) of metoprolol but extensive metabolizers (EMs) of S-mephenytoin (PMML/EMMP), five subjects were EMs of metoprolol but PMs of S-mephenytoin (EMML/PMMP) and seven subjects were EMs of both metoprolol and S-mephenytoin (EMML/EMMP). The mean (+/- S.D.) oral clearances of imipramine were smaller in the PMML/EMMP group and the EMML/PMMP group than in the EMML/EMMP group, although a statistical difference (P < .05) was found only in the EMML/PMMP vs. the EMML/EMMP group. The mean area under the plasma concentration-time curve (AUC) of desipramine was 9 times greater (P < .01) in PMML/EMMP group, whereas the mean value was 0.6 times smaller (P < .05) in the EMML/PMMP group than in the EMML/EMMP group. The log10 metoprolol/alpha-hydroxymetoprolol ratio correlated positively with the AUC of desipramine (P < .01) and with the AUC ratio of desipramine/imipramine (P < .05) but negatively with the AUC ratio of 2-hydroxyimipramine/imipramine (P < .05). Log10 percent 4'-hydroxymephenytoin excreted in 8-hr urine correlated positively with the AUC of desipramine (P < .01) and with the AUC ratio of desipramine/imipramine (P < .01). The urinary excretions of imipramine and its metabolites also reflected the data derived from plasma samples in the three different phenotype-paired panels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

The antagonistic effect of separate and consecutive chronic treatment with imipramine and ECS on the inhibition of alpha 1-adrenoceptor activity by protein kinase C.

We tested how chronic antidepressant treatments (chronic imipramine, chronic electroconvulsive shock (ECS) and chronic ECS given after chronic imipramine) affect the feedback inhibition of alpha 1-adrenoceptor activity (measured with inositol phosphate (IP) accumulation after stimulation with noradrenaline). The inhibitory effect of a 12-O-tetradecanoylphorbol 13-acetate (TPA) on IP response was found to be due to protein kinase C (PKC) activation, as it was abolished by specific protein kinase inhibitors, staurosporine and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7). Chronic ECS completely abolished the inhibition by TPA of inositol phosphate response to noradrenaline, while chronic imipramine reversed the feedback and led to potentiation of responses by TPA to intermediate concentrations of noradrenaline. Subsequent chronic ECS abolished the imipramine-induced reversal of TPA inhibition and lead to the changes similar as observed after ECS alone. The present results may suggest why in some cases, in which imipramine therapy is ineffective, subsequent ECS may be clinically beneficial.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

A double-blind comparison of nefazodone, imipramine, and placebo in major depression.

BACKGROUND: Nefazodone is a 5-HT2-receptor antagonist and serotonin (5-HT) selective reuptake inhibitor. This study evaluates the safety and efficacy of nefazodone in patients with major depressive disorder (MDD) in comparison to imipramine and placebo treatments. It also compares two dose ranges of nefazodone to investigate its optimal dose range. METHOD: Nefazodone was evaluated in a 6-week, double-blind trial of novel design involving 180 patients meeting Research Diagnostic Criteria for major depressive disorder and having a minimum pretreatment score of 22 on the first 17 items of the Hamilton Rating Scale for Depression (HAM-D). Patients were randomly assigned to placebo (2-10 capsules/day), imipramine (50-250 mg/day), or nefazodone in two dose ranges (50-250 mg/day or 100-500 mg/day). RESULTS: Improvement on depression measures with nefazodone in the 100-500-mg/day dose range (endpoint mean = 460 mg/day) and imipramine (endpoint mean = 214 mg/day) exceeded that with placebo. Some benefit was also observed in the nefazodone 50-250-mg/day treatment group (endpoint mean = 242 mg/day), but it was suboptimal. Evidence of nefazodone's efficacy as an antidepressant was consistently observed on physician- (HAM-D, Clinical Global Impressions [CGI]) and patient-rated (CGI-patient rated) scales. By patient self-report, improvement of anxiety symptoms associated with depression was evident with nefazodone as early as the first week of treatment, and benefit was seen with both nefazodone dosage groups. Analyses of the physician's global assessments of therapeutic effect and side effects at end of treatment showed therapeutic benefit for both nefazodone and imipramine treatments; however, patients in the nefazodone treatment groups were significantly less troubled by adverse experiences than were imipramine-treated patients, resulting in a lower dropout rate for adverse experience. CONCLUSION: Nefazodone is a well-tolerated and effective antidepressant for the treatment of major depressive disorder.

Adult↗
PubMed1993

Long-term outcome of panic disorder after short-term imipramine and behavioral group treatment: 2.9-year naturalistic follow-up study.

Twenty-eight patients with a DSM-III diagnosis of agoraphobia with panic attacks who completed a 4-month combined drug and behavioral treatment program and who were then discharged on imipramine were interviewed 1 to 5 years after being discharged. At the time of follow-up, half of the patients were medication free, eight were receiving a lower dose of imipramine, two were receiving the same dose as at the time of discharge, and four patients were receiving other antipanic medications. Panic attack frequency remained reduced at the time of follow-up, as did all anxiety and all impairment ratings. These improvements were similar between patients receiving and not receiving imipramine at this time. Long-term outcome was independent of nonpharmacological therapy during the follow-up interval and lifetime diagnosis of major depression at the time of admission. Our data suggest that improvement observed after 4 months of treatment with imipramine and behavioral therapy is maintained after 1 to 5 years, even for many patients who reduced the dose of or discontinued imipramine. Long-term, randomized studies are needed to compare the efficacy of treatments and to determine treatment duration.

Adult↗
PubMed1993

Neuroanatomical differences in the rate of beta-adrenergic receptor adaptation after repeated treatment with imipramine.

We tested the hypothesis that the time course of neurochemical adaptation that occurs during chronic imipramine treatment varies among specific brain regions. Down-regulation of brain beta-adrenergic receptors was used as a model of antidepressant-induced neural adaptation. Beta-adrenergic receptors were assessed by quantitative autoradiographic analysis of [125I]-pindolol binding after different periods of imipramine treatment. The duration of imipramine treatment required to down-regulate the receptors varied markedly among different brain regions. Select cortical regions exhibited a reduction in [125I]-pindolol binding after only two injections of imipramine. These rapidly adapting cortical regions included the medial prefrontal, ventrolateral orbital, and piriform cortices. In contrast, some brain regions required a 3-week treatment period before down-regulation of beta-adrenergic receptors was observed. Such slowly adapting regions included subdivisions of the hypothalamus and amygdala. Other brain regions examined required intermediate periods of imipramine treatment, of 4 to 14 days, to produce a reduction in beta-adrenergic binding. It is possible that differential rates of neural adaptation among brain regions are related to the time course of therapeutic response to antidepressant drug treatment.

Animals↗
PubMedDate not supplied

The effect of chronic treatment with imipramine on the G proteins mRNA level in the rat hippocampus--an interaction with a calcium channel antagonist.

The effect of long-term administration of imipramine (10 mg/kg po, twice daily, 30 days) with or without nifedipine (5 mg/kg ip, twice daily, 28 days) on the G protein alpha subunit, Gs alpha, Go alpha and Gi alpha mRNA levels was investigated in the rat hippocampus. An in situ hybridization histochemistry showed that imipramine decreased the Go alpha mRNA level in CA1 (by ca. 40%) and CA3 (by ca. 37%) hippocampal fields and, to a lesser extent, in the dentate gyrus (by ca. 25%), but had no effect on the Gs alpha and Gi alpha mRNA levels in those structures. Nifedipine decreased (by ca. 30%) the Gs alpha level in the studied fields of hippocampal formation, having no influence on the level of mRNA which codes other subunits of G protein. Coadministration of nifedipine and imipramine reversed the imipramine effect on Go alpha, but had no effect on the nifedipine-induced decrease at the Gs alpha mRNA level. These results suggest that inhibition of L calcium channels modifies the effect of imipramine at the level of intracellular signal transduction.

Animals↗