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At least 1,369 records · Page 76Linked to original sources
PubMed2001

Short-term effects of three continuous hormone replacement therapy regimens on platelet tritiated imipramine binding and mood scores: a prospective randomized trial.

OBJECTIVE: To evaluate the effects of continuous hormone replacement therapy (HRT) regimens on platelet-tritiated ((3)H-) imipramine binding (Bmax) and mood. DESIGN: Prospective randomized study. SETTING: University hospital. PATIENT(S): Sixty postmenopausal patients. INTERVENTION(S): Randomization to 3 months of daily treatment with tibolone and conjugated equine estrogen (CEE).625 mg combined either with 2.5 or 5 mg of medroxyprogesterone acetate (MPA). The inclusion criteria-matched patients declined for HRT were prescribed daily alendronate. Pre- and posttreatment blood sampling for Bmax and mood evaluation with the Beck Depression Inventory (BDI) and the State-Trait Anxiety Inventory (STAI) were done. MAIN OUTCOME MEASURE(S): Pre- and posttreatment Bmax and mood scores. RESULT(S): As compared with baseline, both CEE+MPA regimens and tibolone significantly increased Bmax. The comparisons of percent change from baseline Bmax for the CEE+MPA and tibolone groups were similar. All three HRT regimens improved the BDI significantly, while there were no significant changes in the STAI. In the alendronate group, there were no significant changes in both pre- and posttreatment Bmax and mood scores. CONCLUSION(S): Continuous treatment with CEE+MPA and tibolone increases platelet (3)H-imipramine binding and improves mood. Mood-enhancing effects of tibolone may occur through the serotonergic system, as is the case with estrogen.

Affect↗
PubMed1981

Reversed-phase liquid chromatography for the separation of chloropromazine, imipramine and some of their metabolites.

Reversed-phase liquid chromatography on a C18 bonded silica with water-alcohol mixtures containing decylamine as the mobile phase was investigated for its applicability to the separation of chlorpromazine, imipramine and their metabolites. The addition of decylamine to the mobile phase was found to be necessary in order to obtain symmetrical peaks. The influence of the decylamine and ethanol concentrations and of the pH of the mobile phase was investigated and these parameters were found to be useful for the adjustment of the retention. The phase system developed was found to be suitable for the required separation. The phase system was applied to the analysis of imipramine and its metabolites, desmethylimipramine and didesmethylimipramine, and desmethylchlorpromazine in human plasma.

Chlorpromazine↗
PubMed1975

Gas chromatographic-mass fragmentographic determation of "steady-state" plasma levels of imipramine and desipramine in chronically treated patients.

A sensitive and specific method for the simultaneous determination of imipramine and desipramine in the blood plasma of depressed patients under treatment that involves separation by gas chromatography and detection by mass fragmentography is described. Concentrations were determined by focusing the mass spectrometer upon the ions at m/e 280 and 235 for imipramine and 308, 236 and 114 for desipramine (N-acetyl derivative), while promazine was used as the internal standard (ions at m/e 284 and 238). Determinations are possible at levels as low as 10 ng/ml in plasma.

Chromatography, Gas↗
PubMedDate not supplied

Adrenergic receptor function in panic disorder. II. Neutrophil beta 2 receptors: Gs protein coupling, effects of imipramine treatment and relationship to treatment outcome.

Panic attacks are associated with increased autonomic symptoms, suggesting increased beta 2-adrenergic receptor (beta 2AR) function in PD. Tricyclic antidepressants downregulate beta AR function. Previous studies on beta AR function in PD, however, are inconsistent. We recently found increased beta AR coupling and density in neutrophils of symptomatic drug-free PD patients. This study evaluated beta AR coupling to Gs protein in 28 controls, 25 drug-free PD patients and 8 PD imipramine-treated patients. PD patients had significantly higher coupling and receptor density, particularly in the high-conformational state. Differences were more pronounced in patients with less depressive symptomatology. Treatment with imipramine was associated with decreased beta AR coupling and density in the high-conformational state. Several beta AR binding parameters were related to severity of anxiety symptoms and treatment outcome. Antidepressants downregulate beta AR density and induce uncoupling from Gs protein in PD. Future studies may investigate beta AR coupling in relationship to treatment outcome and the role of beta AR kinase in PD.

Adrenergic beta-Antagonists↗
PubMed1975

Imipramine toxicity.

Clinical experience has firmly established the usefulness of imipramine in the management of enuresis. Our report describes the serious dose-related cardiac and central nervous system toxic effects of imipramine. Comparison of the human and animal toxicity data is presented and recommendations are given for safe human dose ranges.

Animals↗
PubMed2001

Repeated treatment with imipramine, fluvoxamine and tranylcypromine decreases the number of escape failures by activating dopaminergic systems in a rat learned helplessness test.

Chronic administration of antidepressants has been shown to reduce the number of escape failures in the rat learned helplessness test (LH). In the present study we investigated the role of D1, D2 and D3 receptors in mediating this effect. In our first series of experiments, we demonstrated that SKF38393, D1 receptor agonist, in a dose of 2.5 mg/kg (i.p.) and quinpirole, D2 receptor agonist in a dose of 0.5 mg/kg (i.p.), significantly decreased the number of escape failures in LH, and these were reversed by SCH23390 (0.015 mg/kg), D1 receptor antagonist, and by sulpiride (25 mg/kg), D2 receptor antagonist, respectively. In contrast, 7-OH-DPAT, a D3 receptor agonist, in a dose of 10 mg/kg (i.p.) did not affect the number of escape failures in LH. In a second series of experiments, we showed that eight days of repeated treatment with imipramine (10 mg/kg, p.o.), fluvoxamine (1.25 mg/kg, p.o.) and tranylcypromine (1.25 mg/kg, p.o.) significantly decreased the number of escape failures in LH. The decrease in escape failures seen with use of imipramine and tranylcypromine was reversed by sulpiride in LH, but not by SCH23390. On the other hand, the effect of fluvoxamine was reversed by both SCH23390 and sulpiride. These findings indicate that stimulation of D1 and D2 receptors decreased the number of escape failures in LH, respectively. Thus, D2 and/or D1 receptors are probably involved in the decreased number of escape failures in case of repeated treatment with antidepressants in LH.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1983

Inhibitory effect of imipramine on epinephrine-dependent platelet aggregation: "in vitro" studies on platelets from healthy and depressed people.

Inhibitory effect of imipramine on platelet aggregation in healthy and depressed people was studied. A different sensitivity was observed between healthy and depressed people. Two groups (D I and D II) were identified among depressed patients on the basis of sensitivity to imipramine effect. ID50 was calculated for healthy subjects (59.5 +/- 22 microM) and depressed patients (D I: 20 +/- 7 microM - D II: 117 +/- 49).

Adult↗
PubMed1983

Action of caffeine, d-amphetamine, diazepam and imipramine in a dynamic behavioural situation.

A study has been made of how the chronic administration of caffeine, d-amphetamine, imipramine and diazepam affect rat behaviour in four successive trials in which the contingency for food delivery was switched from one lever where responses were previously reinforced to the other lever where responses had no programmed consequences (reversal). A complete extinction in the first reversal was obtained with diazepam 0.3 mg/kg/day. Caffeine (6 and 18 mg/kg/day) had no effect in the first reversal and damaged rat performance in the successive reversals. Imipramine (0.6 and 4 mg/kg/day) had the same effect but only in the fourth reversal. Amphetamine (0.16 and 0.7 mg/kg/day) caused a clear damage of rat performance only in the third and fourth reversals.

Animals↗
PubMedDate not supplied

Antimalarial effect in vitro and lack of modulating effect of desipramine and imipramine.

Based on previous studies in vitro of the modulating effect of desipramine on chloroquine-resistance of Plasmodium falciparum, the effect of desipramine and imipramine on freshly isolated resistant Brazilian strains of the parasite was investigated. Both drugs in therapeutic doses showed an unexpected antimalarial effect in vitro in duplicate tests (IC50 = 44.26 and 46.53 micrograms/L for desipramine, and 83.93 and 41.26 micrograms/L for imipramine), but no reversal of resistance when added to cultures together with chloroquine.

Animals↗
PubMed1997

Amisulpride versus imipramine and placebo in dysthymia and major depression. Amisulpride Study Group.

Amisulpride, a selective antagonist of D2 and D3 dopamine receptors, acts preferentially on presynaptic receptors increasing dopaminergic transmission at low doses. In a multicentre, 6 months, placebo-controlled trial, amisulpride (50 mg/daily) was compared to imipramine (100 mg/daily) in the treatment of patients with DSM-III-R criteria for primary dysthymia, dysthymia with major depression or major depression in partial remission. A total of 219 patients were included. Both analyses (intention-to-treat and "per protocol' analysis) detected significant differences between groups (active treatment vs. placebo) on all main rating scales (CGI, MADRS, ERD, and SANS). The number of patients reporting at least one adverse event was higher in the imipramine group than in the two other, mainly due to anticholinergic effects. Endocrine symptoms were more frequent in female patients treated with amisulpride. These results confirm the interest of a drug acting on dopaminergic transmission such as amisulpride in the treatment of depressed patients.

Adult↗
PubMed1999

Platelet alpha2A-adrenoceptor function in major depression: Gi coupling, effects of imipramine and relationship to treatment outcome.

Studies suggest alpha2A-adrenoceptors (alpha(2A)AR) dysregulation in major depressive disorder (MDD). Platelet alpha(2A)ARs exist in high- and low-conformational states that are regulated by Gi protein. Although alpha(2A)AR coupling to Gi protein plays an important role in signal transduction and is modulated by antidepressants, it has not been previously investigated. Alpha2AR density in the high- and low-conformational states, agonist affinity and coupling efficiency were investigated in 27 healthy control subjects, 23 drug-free MDD patients and 16 patients after imipramine treatment using [3H]yohimbine saturation and norepinephrine displacement of [3H]yohimbine binding experiments. Coupling measures were derived from NE-displacement experiments. Patients had significantly higher alpha(2A)AR density, particularly in the high-conformational state, than control subjects. Coupling indices were normal in patients. High pre-treatment agonist affinity to the receptor in the high-conformational state and normal coupling predicted positive treatment outcome. Decreased coupling to Gi predicted a negative treatment outcome. Imipramine induced uncoupling (-11%) and redistribution of receptor density in treatment responders only, but had no effect on alpha(2A)AR coupling or density in treatment non-responders. Increased alpha(2A)AR density may represent a trait marker in MDD. The results provide indirect evidence for abnormal protein kinase A (PKA) and protein kinase C (PKC) in MDD which may be pursued in future investigations.

Adrenergic Uptake Inhibitors↗
PubMed1994

Magnesium potentiates imipramine toxicity in the isolated rat heart.

STUDY OBJECTIVE: To study the effect of magnesium on cardiac function and hemodynamics during imipramine toxicity. DESIGN: After stabilization, isolated, beating rat hearts were perfused with Krebs-Henseleit bicarbonate buffer (KHB) solution containing 2.0 mg/L imipramine (IMIP) and 2.4 mEq [Mg2+] until toxicity, defined as 25% widening of the ventricular depolarization duration (VDD). Experiments were performed at either constant coronary perfusion pressure or flow. SETTING: Animal research laboratory of a large, urban hospital. MEASUREMENTS: Heart rate, VDD, left ventricular pressure and +/- dP/dt, and coronary flow. INTERVENTIONS: On onset of toxicity, KHB+IMIP was switched to either control (KHB+IMIP), magnesium (KHB+IMIP+4.0 or 6.0 mEq/L [Mg2+]), or hypertonic alkaline treatment (165 mEq/L [Na+], pH 7.55). RESULTS: At a constant coronary perfusion pressure of 100 mm Hg, magnesium at 6.0 mEq produced significant decreases in heart rate, left ventricular pressure, +dP/dt, and increase in VDD versus control. With coronary flow held constant, magnesium reduced left ventricular pressure and +dP/dt but not heart rate or VDD. Incidences of electromechanical dissociation and asystole were higher with magnesium versus control. Hypertonic alkaline treatment tended to improve all parameters in constant pressure and constant flow experiments. CONCLUSION: Magnesium potentiates IMIP-induced negative inotropic effects and cardiac conduction defects in isolated rat hearts.

Animals↗
PubMed1997

Chronic imipramine treatment upregulates IR2-imidazoline receptive sites in rat brain.

A low density of brain IR2-imidazoline receptive sites has previously been linked to depression. In this study we evaluated brain IR2-binding sites in a rat model of depression, olfactory bulbectomy, and determined the effects of chronic imipramine treatment in vivo on these sites. Compared with sham-operated controls, adaptation to olfactory bulbectomy had no effect on either the density (Bmax) or affinity (KD) of [3H]-idazoxan binding to brain IR2 sites. However, 25 days of imipramine treatment (i.p., 20 mg/kg/day) enhanced significantly the density of IR2 binding sites, with no change in affinity in both the model and the control group. These results indicate that the brain IR2-imidazoline receptive sites might be a target for antidepressants.

Animals↗
PubMed1987

Influence of imipramine and chloroquine on lung phospholipid content and lung structure in newborn rats.

In continuation of previous experiments in adult rats the alteration in content and composition of lung phospholipids (PL) and lung structure of newborn rats of different gestational age was studied after three administrations of the amphiphilic drugs imipramine (75 mg/kg b.w.) and chloroquine (50 mg/kg b.w.). The fetuses were obtained by Cesarean section on day 20, 21, or 22 of gestation. Morphological examinations of the lungs of drug treated 21-day-old fetuses revealed a substantially better aeration than nontreated controls. 20 and 22 days old fetuses showed no differences in aeration between drug and saline treated rats. Analogous results were obtained with respect to the 1 h survival rate of newborns. Furthermore, imipramine and chloroquine cause a premature development of the pneumocytes type II as shown by electron microscopy. An increased PL content as well as disaturated phosphatidylcholine (DSPC) and phosphatidylglycerol (PG) proportion of fetal lungs, especially in animals born on day 21 of gestation, were found after drug treatment. The results suggest an acceleration of maturation of the pneumocytes type II in fetal lungs induced by amphiphilic drugs.

Animals↗
PubMed2001

Chronic imipramine treatment partially reverses the long-term changes of hippocampal synaptic plasticity in socially stressed rats.

In the present study, we investigated whether synaptic plasticity changes in the hippocampus of depressive-like socially stressed rats could be reversed by chronic antidepressant treatment. To that end, rats were either defeated and subsequently individually housed or subjected to control treatment followed by social housing. After a period of at least 3 months, rats were either treated chronically with imipramine (20 mg/kg per day, per os for at least 3 months) or the solvent solution (i.e. water). Then, long-term potentiation and depression were measured in the CA1 region of the hippocampus in vitro. Chronic imipramine treatment partially restored the attenuated induction of long-term potentiation and suppressed the facilitation of long-term depression-induction in socially stressed rats. The altered synaptic plasticity after social stress is discussed in relation to cognitive deficits and hippocampal changes that are observed in depressive patients.

Animals↗
PubMed1999

Effects of chronic mild stress (CMS) and imipramine administration, on spleen mononuclear cell proliferative response, serum corticosterone level and brain norepinephrine content in male mice.

There is increasing evidence that stress and emotional reactions produce changes in various immune processes. These changes may be due to alterations of the stress responses endocrine and for autonomic mediating mechanisms. In order to study such effects, the impact of chronic mild stress (CMS) application, and of subsequent imipramine administration were studied on the spleen mononuclear cell proliferative response period. OFI strain male mice were subjected to 4 or 7 weeks of CMS. The effects of these treatments on serum corticosterone levels and hypothalamic and hippocampal norepinephrine (NE) contents were also assessed. Subjects submitted to CMS had a higher spleen mononuclear cell proliferative response after either treatment duration. Imipramine treatment diminished this response enhancement in CMS exposed animals, but did not alter the proliferative responses of control subjects. Serum corticosterone levels, as well as hypothalamic and hippocampal nonrepinephrine contents did not significantly vary between groups. Taken together, these results suggest that CMSs effects on immune reactivity are not related to serum glucocorticoids or NE changes in these locations associated with the hypothalamic-pituitary- adrenocortical (HPA) axis.

Adrenergic Uptake Inhibitors↗
PubMed2002

Sister chromatid exchanges produced by imipramine and desipramine in mouse bone marrow cells treated in vivo.

Imipramine and desipramine are two widely used tricyclic antidepressants which have shown conflicting results in regard to their in vitro genotoxic evaluation. The aim of this investigation was to determine the capacity of these compounds to induce in vivo sister-chromatid exchanges (SCEs) in mouse bone marrow cells. For each compound, the animals were organized in five groups constituted by five individuals. They were intraperitoneally (ip) administered with the test substances as follows: a negative control group treated with 0.4 ml of distilled water, a positive control group administered with cyclophosphamide (70 mg/kg), three groups treated with imipramine (7, 20 and 60 mg/kg), and three other groups treated with desipramine (2, 20 and 60 mg/kg). The general procedure included the subcutaneous implantation to each mouse of a 5-bromodesoxyuridine tablet (45 mg), and 1 h later, the administration of the chemicals involved. Twenty-one hours after the tablet implantation, the mice received colchicine, and 3 h later their femoral bone marrow was obtained in KCL, fixed, and stained with the Hoechst-Giemsa method. The results showed that both compounds were SCE inducers, starting from the second tested dose. The response of these compounds was dose-dependent, and showed that the highest tested dose increased about four times the SCE control level. The cellular proliferation kinetics was not affected by the chemicals, and the mitotic indexes were slightly diminished with the highest dose. These results indicate an in vivo genotoxic potential for both chemicals, and suggest that it is pertinent to follow their evaluation in other models.

Animals↗