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PubMedDate not supplied

Response of panic disorder to fixed doses of alprazolam or imipramine.

This paper reports the results of a double-blind comparison of fixed daily doses of 6 mg of alprazolam, 2 mg of alprazolam, 225 mg of imipramine, and placebo for 8 weeks in 81 patients who met DSM-III criteria for panic disorder with or without agoraphobia. Final scores on eight clinical measures were analyzed from all patients who entered the study and from the subset who completed at least 4 weeks of treatment. Eighty-six percent of the high-dose alprazolam patients completed the study. Only 50% of the imipramine patients completed 8 weeks of treatment, apparently because of activation early in treatment and slow onset of therapeutic effects. This study confirmed the therapeutic effectiveness and safety of alprazolam, especially at the higher dose, in panic disorder. It also confirmed the therapeutic effectiveness of imipramine among patients who tolerated the drug. It suggested the usefulness of a flexible, individual approach to dose escalation with imipramine. Methodologically the study underscored the importance of using multiple approaches to the analysis of clinical data from therapeutic trials of psychotropic agents with complex effects that may contribute to patients' premature termination.

Agoraphobia↗
PubMed1996

Quantitative EEG in the prediction of antidepressant response to imipramine.

The purpose of this study was to examine the utility of quantitative electroencephalography (QEEG) in the prediction of response to imipramine in depressed patients. Forty patients with a diagnosis of unipolar depression were subjected to a placebo washout and were assessed at pre-drug, 3 h after their first dose of imipramine, and again 2 weeks into treatment. Following 4 weeks of open imipramine treatment, patients were separated into responder (R) and non-responder (NR) groups. Statistical analysis of the 29 patients who completed the study focused on group comparisons of power spectral estimates in four frequency bands from multi-channel recordings. Results showed that theta power differentiated R and NR groups prior to treatment, in response to an acute test dose, as well as after 2 weeks of active drug treatment. Results based on this exploratory study suggest that QEEG may be a useful early predictor of response to imipramine.

Adult↗
PubMed1984

High-affinity 3H-imipramine binding in platelets of children and adolescents with major affective disorders.

High-affinity 3H-imipramine binding to platelet membranes was evaluated in 12 untreated children and adolescents aged 11-17 years who met the DSM-III criteria for major affective disorders. The affective patients were compared to 13 nonaffective subjects and 15 normal controls of similar ages. No significant difference in the maximal binding of 3H-imipramine (Bmax) and Kd values could be found among the three groups. 3H-Imipramine binding values failed to discriminate between patients with major depression and those with bipolar disorder, depressed type. No association between a positive family history of major affective disorders and 3H-imipramine binding values was detected.

Adolescent↗
PubMed1985

3H-Imipramine binding sites in platelets of hospitalized psychiatric patients.

The density of platelet 3H-imipramine binding sites has been proposed as a biological marker in psychiatry. We report the range of platelet 3H-imipramine binding in 55 psychiatric patients and 11 control subjects. All blood samples were withdrawn at 2300 h (on the day of hospital admission for patients). With the use of a slight modification of a previously described 3H-imipramine binding method, a mean B max of 1,510 fmole/mg protein (range: 390-5,560; median: 1,450) and a mean Kd of 2.0 nM (range: 0.6-17.0; median: 1.4) were determined for psychiatric patients. For the controls, a mean B max of 1,590 fmole/mg protein (range: 870-2,570; median: 1,440) and a mean Kd of 1.4 nM (range 0.8-2.4; median 1.4) were determined. When patients were subdivided based on ICD-9 psychiatric diagnoses, no significant differences between distinct subgroups of psychiatric patients with respect to B max or Kd values for platelet 3H-imipramine binding could be established. Similarly, no significant difference between psychiatric patients and controls was obtained.

Adolescent↗
PubMed1986

Imipramine binding sites on platelets of patients with major depressive disorder.

3H-Imipramine binding to platelets of patients with primary, unipolar major depressive disorder was investigated and compared to that of a normal, healthy control population. No significant differences could be demonstrated between either the Kd or the Bmax values of the two groups. A negative correlation was observed between imipramine Bmax values and the Hamilton anxiety ratings of the depressed patients. Patients who displayed psychomotor retardation tended to have lower platelet imipramine Bmax values than patients with psychomotor agitation. It is suggested that platelet imipramine Bmax values may be a biological marker for subtypes of depression.

Adult↗
PubMed1986

Reduced 3H-imipramine binding but unaltered 3H-serotonin uptake in platelets of adolescent enuretics.

High affinity 3H-imipramine binding and 3H-serotonin uptake to platelets was evaluated in nine untreated adolescent enuretics (ages 13-18) and nine age- and sex-matched controls. A significant decrease in the maximal binding of 3H-imipramine (Bmax) was observed in the enuretics as compared to the controls. No alteration in the affinity of 3H-imipramine to its binding sites (Kd) or in serotonin uptake kinetic parameters (Vmax, Km) was detected. The lack of correlation between Bmax and Vmax values might indicate that the binding sites for imipramine and the sites for serotonin uptake are not identical.

Adolescent↗
PubMed1988

A longitudinal study of intact platelet 3H-imipramine binding in 12 normal human subjects.

Most investigators have measured binding of 3H-imipramine to platelet membranes, but some of the preparations may have contained varying proportions of intracellular protein because of contamination with incompletely lysed platelets. Since binding to membranes has been expressed with reference to the amount of protein in the membrane preparation, it is not surprising that there are discrepancies and a wide range of reported values for platelet imipramine binding in the literature. We have now completed a 9-month study of the binding of 3H-imipramine to intact platelets obtained monthly from 12 normal subjects. Using the intact platelet assay, as described by Friedl and Propping, we found that both Bmax and Kd for 3H-imipramine binding exhibited large month-to-month variations and no consistent seasonal trend was observed. The substantial variation in both Bmax and Kd among normal subjects and among samples obtained from the same individual at different times may limit the clinical usefulness of these measurements. A single blood sample is unlikely to give reliable values for Bmax and Kd for comparison purposes.

Adult↗
PubMed1988

Platelet tritiated imipramine binding and MAO activity in Alzheimer's disease patients with agitation and delusions.

Decreased platelet 3H-imipramine binding density and decreased monoamine oxidase (MAO) activity have been considered as biological characteristics of several neuropsychiatric disorders, and may be related to central serotonin defects. Since serotonin system defects occur in Alzheimer's disease (AD), and decreased brain 3H-imipramine binding density, and increased brain and platelet MAO activity are reported also, we studied platelet 3H-imipramine binding density (Bmax) and platelet MAO activity in AD outpatients without antecedent psychiatric disorder. AD subjects with significant symptomatic behavioral disorder, predominantly agitation and delusions, and AD subjects without symptomatic behaviors were compared with controls. Age, sex, mini-mental state examination score, and illness duration did not distinguish the two AD groups. The agitated/delusional group showed significantly lower Bmax values than uncomplicated AD subjects or controls. MAO activity was significantly increased among female AD subjects without symptomatic behaviors compared to those who were agitated or to controls. These results indicate that 3H-imipramine binding and MAO activity may distinguish AD subjects with agitation or delusions from those without symptomatic behaviors, and suggest the existence of a biologically based Alzheimer's behavioral subtype.

Aged↗
PubMed1990

Regional distribution of the serotonin transport complex in human brain, identified with 3H-paroxetine, 3H-citalopram and 3H-imipramine.

1. Regional distribution of the serotonin transport complex was studied in 12 different brain areas from human brains. The serotonin uptake complex was measured with 3H-paroxetine, and 3H-imipramine. The binding site density was highest in the nucleus of raphé, medium in the basal ganglia, and lowest in cortical areas. The specific binding measured with 3H-paroxetine and 3H-citalopram was compared with the high affinity 3H-imipramine binding determined with either 100 microM 5HT or 1 microM imipramine as non specific displacers. 3H-paroxetine and 3H-citalopram allowed a more precise determination of Bmax, and are both good ligands for the serotonin uptake site, but the determinations with 3H-imipramine were within the same range. 2. Protease digestion of brain membranes showed that the binding site measured with all three ligands disappeared with the same rate as other membrane proteins, and not faster as might be expected from the literature. 3. Left/right hemisphere distribution was measured in cortical tissue from 6 brains using 3H-paroxetine. No difference between the two hemispheres was found. In one brain from a lithium treated patient a very low binding was measured, possibly indicating that the lithium treatment had decreased the serotonin uptake mechanism.

Adolescent↗
PubMed1992

Adjunctive imipramine for dysphoric schizophrenic patients with past histories of cannabis abuse.

1. Twenty-one schizophrenic or schizoaffective patients with histories of cannabis abuse and operationally-defined syndromes of post-psychotic depression completed a double-blind trial of adjunctive imipramine added to their on-going medication regimen of fluphenazine decanoate and benztropine. 2. The imipramine-treated patients had superior global outcome. 3. Subscales suggested that specific improvement occurred in imipramine-treated patients in the domain of depression-like features. 4. Psychotic symptomatology was not found to be exacerbated by the imipramine.

Adolescent↗
PubMed1981

Beta-adrenergic receptors in rat cerebellum after neonatal X-irradiation: effect of prolonged imipramine and lithium treatment.

The actions of prolonged treatment of rats within imipramine or lithium chloride on the beta-adrenergic cAMP generating system of the cerebellum were compared in normal animals and in rats degranulated by neonatal X-irradiation. Whereas in normal animals imipramine treatment is without significant effect on the cerebellar cAMP system but lowers the beta-adrenoceptor density significantly, in degranulated animals the cAMP system becomes subsensitive towards norepinephrine after prolonged imipramine treatment. These data support the hypothesis that in the cerebellum imipramine acts predominantly on beta-adrenoceptors located particularly on Purkinje cells. Prolonged lithium treatment exhibited no significant effects on beta-receptors nor the noradrenergic cAMP generating system of normal and degranulated cerebella.

Animals↗
PubMed1990

Thyrotropin and prolactin responses to protirelin (TRH) prior to and during chronic imipramine treatment in patients with panic disorder.

The effects of protirelin [thyrotropin-releasing hormone (TRH)] administration on the release of thyrotropin (TSH) and prolactin (PRL) were examined in 14 patients with panic disorder prior to and during chronic treatment with imipramine. During imipramine treatment, the patients exhibited an increase in their TSH response to TRH (delta delta max TSH = 3.65 +/- 6.02 mu IU/ml, p less than 0.05) and in their PRL response to TRH (delta AUCPRL = 734 +/- 965 ng/ml/45 min, p less than 0.005). Several behavioral measures correlated with the neuroendocrine measures during imipramine therapy. These preliminary findings might suggest a role for changes in dopaminergic function in the clinical effects of imipramine in patients with panic disorder.

Adult↗
PubMed1991

Determination of imipramine, desipramine and their hydroxy metabolites by reversed-phase chromatography with ultraviolet and coulometric detection.

A reversed-phase high-performance liquid chromatographic method is described which analyzes imipramine, desipramine and their corresponding 2-hydroxy metabolites with sequential ultraviolet and coulometric detection from a single common extraction step, so that a wider dynamic range of plasma concentrations can be measured requiring smaller sample volumes. Applicability is broader including single-dose pharmacokinetic studies as well as steady-state concentrations. The extraction procedure gives excellent recoveries for imipramine, desipramine and their metabolites (mean +/- S.D.): ultraviolet detection, imipramine 99.5 +/- 0.68%, desipramine 100 +/- 0.0%, 2-hydroxyimipramine 97.8 +/- 3.5% and 2-hydroxydesipramine 93.1 +/- 4.22%; coulometric detection, imipramine 97.5 +/- 1.9%, desipramine 98.3 +/- 1.2%, 2-hydroxyimipramine 90.3 +/- 4.0% and 2-hydroxydesipramine 86.6 +/- 7.5%.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

The use of imipramine in minor motor seizures.

A study is presented of 15 pediatric patients treated with imipramine for uncontrolled seizures during the past two years. Of these patients, 53% had an initial reduction of seizures of greater than 80%. At one year, 26% were still seizure-free. Drop attacks were especially responsive to therapy; 100% (7/7) responded initially to imipramine therapy. Most patients studied had been receiving valproate and another major antiepileptic drug prior to imipramine therapy. This study confirms previous reports and suggests that the use of imipramine in combination with other antiepileptic drugs provides excellent results, particularly in patients with drop attacks.

Adolescent↗
PubMed2005

Imipramine and citalopram facilitate amyloid precursor protein secretion in vitro.

Comorbid depression of Alzheimer's disease (AD) is a common mood disorder in the elderly and a broad spectrum of antidepressants have been used for its treatment. Abeta peptides and other derivatives of the amyloid precursor protein (APP) have been implicated as central to the pathogenesis of AD. However, the functional relationship of APP and its proteolytic derivatives to antidepressant therapy is not known. In this study, Western blotting was used to test the ability of the tricyclic antidepressant (TCA) imipramine or the selective serotonin reuptake inhibitor (SSRI) citalopram to change the release of APP and the protein kinase C (PKC) content. Both antidepressants increased APP secretion in primary rat neuronal cultures. Imipramine or citalopram enhanced the level of secreted APP by 3.2- or 3.4-fold, respectively. Increases in PKC level were observed only after imipramine treatment. These in vitro data suggest that both TCA and SSRI are able to interfere with the APP metabolism. Imipramine promotes the non-amyloidogenic route of APP processing via stimulatory effects on PKC. We propose that PKC is not involved in the mechanism underlying the effects of citalopram on the APP metabolism. Since the secreted APP is not further available for the pathological cleavage of beta- and gamma-secretases, antidepressant medication might be beneficial in AD therapy.

Alzheimer Disease↗
PubMed1998

Mechanism of the inhibitory effect of imipramine on the Na+-dependent transport of L-glutamic acid in rat intestinal brush-border membrane.

The mechanism of the inhibitory effect of imipramine, a lipophilic organic cation on the Na+-dependent transport of L-glutamic acid across intestinal brush-border membrane was investigated. The uptake of L-glutamic acid by intestinal brush-border membrane vesicles was dependent on the concentration of Na+. Fitting of the uptake data in the presence of various concentrations of Na+ using Hill equation yielded a Hill coefficient of 2.18. This result suggest that the carrier system of L-glutamic acid has at least two sites for Na+-binding. By the analysis of double reciprocal plot and Dixon-type plot, it was found that imipramine inhibits the transport of L-glutamic acid by interacting competitively with the binding sites of Na+, but not inhibit L-glutamic acid binding site. Moreover, the effect of imipramine on the transport of L-alanine and D-glucose which are co-transported with only one Na+ molecule was also suggestive of interaction with the Na+-binding sites on the carrier. These results indicate that the mechanism of the inhibitory effect of imipramine on the Na+-dependent carrier systems is common for all systems regardless of the stoichiometry or substrates.

Alanine↗
PubMed1978

Nanogram-range determination of plasma imipramine by gas-liquid chromatography using a selective nitrogen/phosphorus detector.

A sensitive and specific gas chromatographic method for the quantitative determination of plasma concentrations resulting from a single normal therapeutic dose of imipramine has been developed and is descriged. After extraction into a mixture of n-heptane/isoamyl alcohol (98.5:1.5), imipramine is well separated from its main metabolite, desmethylimipramine, and both compounds are detected using a selective detector operating in the N/P mode. The procedure permits the rapid routine quantitative analysis of relatively small plasma volumes (1-2 ml) containing as little as 1-2 ng of imipramine. No interference from the biological matrix is apparent. The suitability of the method for the analysis of biological samples was tested by studying the time of course of imipramine plasma concentrations in normal human volunteers, after administration of a single therapeutic dose.

Chromatography, Gas↗
PubMed2001

Effects of 5-HT(2) receptor antagonists on the anti-immobility effects of imipramine in the forced swimming test with mice.

The effects of 5-HT(2) receptor antagonists on antidepressant effects of imipramine were investigated in the forced swimming test. Imipramine induced anti-immobility effects in mice dose dependently. Pretreatment with the 5-HT(2A/2B/2C) receptor antagonist, 4-isopropyl-7-methyl-9-(2-hydroxy-1-methyl-propoxycarbonyl)-4,6A,7,8,9,10,10A-octahydro-indolo[4,3-FG]quinolone maleate (LY 53857) significantly enhanced the anti-immobility effects of imipramine. The 5-HT(2C/2B) receptor antagonist, N-3-pyridinyl-3,5-dihydro-5-methyl-benzo[1,2-b:4,5-b']dipyrrole-1(2H)-carboxamide (SB 206553), also enhanced, while the 5-HT(2A) receptor antagonist, ketanserin, was without effect. These results suggest that blockade of the 5-HT(2C/2B) receptor leads to potentiation of the antidepressant effects of imipramine.

Animals↗