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PubMed2002

Imipramine hydrochloride and desipramine hydrochloride as new reagents for detection of microamounts of blood in urine.

Benzidine and o-tolidine, the hazardous carcinogens are still in use for the detection of blood in urine. Development of safer substitutes are of paramount importance. Unfortunately, the alternate available reagents lack specificity, sensitivity and reproducibility. Imipramine hydrochloride (IPH) and desipramine hydrochloride (DPH) are proposed as new reagents for the detection of blood in urine. Both the reagents impact to blood a green-blue to blue color, in the presence of acetic acid and hydrogen peroxide and the development of this color is explored under laboratory conditions. IPH or DPH compares favorably with benzidine and multistix methods. Both the reagents are relatively inexpensive, and have required sensitivity and stability. The proposed reagents offer advantages of relatively low sensitivity to endogenous vegetable peroxidases; hence, the test can be performed on samples taken from patients who are on a normal diet and the results are reproducible. Besides, the reagents, are non-carcinogenic and can replace benzidine and o-tolidine without any extra procedural difficulties as they also exhibit a similar blue color.

Acetates↗
PubMed2002

Studies and analytical application of reaction of imipramine with chrome azurol S.

Chrome azurol S (CAS) was tested as a spectrophotometric reagent for the determination of imipramine (IMP). It reacts in aqueous media with IMP forming pink-red, sparingly soluble in water ion association compound. This compound was quantitatively extracted with chloroform and the absorbance of organic phase was measured at 510 nm. The extraction conditions were studied using a batch method. On the basis of the results obtained with batch method, three-line flow-injection system was constructed. Batch and flow-injection methods were successfully applied for the determination of IMP in pharmaceutical preparation.

Hydroxybenzoates↗
PubMed1996

Voltammetric determination of imipramine hydrochloride and amitriptyline hydrochloride using a polymer-modified carbon paste electrode.

In this paper the voltammetric behaviors of imipramine.HCl and amitriptyline. HCl, which are both tricyclic antidepressants, were investigated using a carbon paste electrode, modified by the addition of poly(N-vinylimidazole), in various solutions of different pHs. It was shown that the current density for imipramine increased with modification of the carbon paste electrode and amitriptyline, which was electroinactive with the normal carbon paste electrode, became electroactive on the modified electrode. The optimum conditions for the quantitive determination of imipramine.HCl and amitriptyline.HCl were determined and statistical analysis of the linear relationship between current and concentration is given. The method was applied for the determination of these substances in the pharmaceutical dosage forms.

Amitriptyline↗
PubMed2002

Postnatal maternal deprivation aggravates experimental autoimmune encephalomyelitis in adult Lewis rats: reversal by chronic imipramine treatment.

Stressful experiences can modulate multiple sclerosis, but stress protection is currently not considered a treatment option. Here, we show that maternal deprivation, an adverse stress experience in infancy, increases emotionality in behavioral tests of adult female Lewis rats and concomitantly causes a more severe course of experimental autoimmune encephalomyelitis. Treatment of these effects in adulthood by chronic antidepressants (imipramine) reversed the behavioral symptoms and attenuated the course of the encephalomyelitis in deprived rats. Increased IL-4 plasma levels accompanied the protective-like effects of antidepressants. In contrast, attempts to prevent these effects in infancy by tactile stimulation aggravated the encephalomyelitis, possibly by decreasing corticosterone and increasing IFN-gamma levels during the disease. This indicates that antidepressants exert protective effects in an animal model of multiple sclerosis, and suggests that drugs modifying stress responsiveness may have a potential role as adjuvant treatment of the disease.

Animals↗
PubMed2000

Adjunctive imipramine for a broader group of post-psychotic depressions in schizophrenia.

As an expansion of work examining the usefulness of adjunctive imipramine added to fluphenazine decanoate and benztropine in the treatment of post-psychotic depression, a previously successful and informative protocol was extended to a larger and more heterogeneous cohort of clinic and day-treatment patients. Although the benefit of the adjunctive antidepressant strategy was still observable in the total sample, as calculated by the prospectively intended data analysis, the findings were weaker than those obtained for the initial cohort. Owing to the possibility that differences between the later and earlier cohorts might account for the muted nature of the benefit, a post-hoc analysis was undertaken. This revealed that the later cohort was sicker in general and more psychotic in particular. The later cohort was also treated with lower doses of neuroleptic medication while remaining out of hospital longer, consistent with more recent treatment trends. It was also possible that the later cohort was subtly selected for more refractoriness of depression, since treatment of post-psychotic depression with adjunctive antidepressants had become more commonplace, and patients responding to this in general practice would not have gone on to be referred to the study. Thus a benefit from adjunctive antidepressant medication persists, but more remains to be learned about its character and likelihood in specific situations.

Adult↗
PubMed2003

Fatal interaction between tranylcypromine and imipramine.

This case report describes a patient on tranylcypromine who erroneously received a single dose of imipramine and subsequently developed a fatal serotonin syndrome. Both the clinical features and the pathophysiology of the serotonin syndrome are discussed.

Adrenergic Uptake Inhibitors↗
PubMed1993

Cardiac toxicity in an adolescent following chronic lithium and imipramine therapy.

A case report is presented of an adolescent male who developed hypothyroidism and cardiomyopathy 6 months after he began taking lithium and imipramine for a severe conduct disorder. After discontinuation of psychiatric medications and institution of thyroid hormone replacement therapy, he developed asymptomatic but potentially serious dysrhythmias. Evidence for potential cardiac toxicity of combined lithium and tricyclic antidepressant therapy is reviewed. Repeated assessment of cardiac function during such therapy is advised.

Adolescent↗
PubMed2002

A double-blind, randomized parallel-group, efficacy and safety study of intramuscular S-adenosyl-L-methionine 1,4-butanedisulphonate (SAMe) versus imipramine in patients with major depressive disorder.

S-adenosyl-L-methionine (SAMe) is a natural substance which constitutes the most important methyl donor in transmethylation reactions in the central nervous system. Several clinical trials have shown that SAMe possesses an antidepressant activity. This multicentre study was carried out to confirm both efficacy and safety of SAMe in the treatment of major depression. SAMe was given intramuscularly (i.m.) at a dose of 400 mg/d, double-blind, vs. 150 mg/d oral Imipramine (IMI) in patients with a diagnosis of major depressive episode, with a baseline score on the 21-item Hamilton Depression Rating Scale (HAMD) of >or=18. A total of 146 patients received SAMe whereas 147 received IMI for a period of 4 wk. The two main efficacy measures were endpoint HAMD score and percentage of responders to Clinical Global Impression (CGI) at week 4. Secondary efficacy measures were the final Montgomery-Asberg Depression Rating Scale (MADRS) scores and the response rate intended as a fall in HAMD scores of at least 50% with respect to baseline. The analysis of safety and tolerability was conducted in all treated patients. SAMe and IMI did not differ significantly on any efficacy measure, either main or secondary. Adverse events were significantly less in patients treated with SAMe compared to those treated with IMI. These data show 400 mg/d i.m. SAMe to be comparable to 150 mg/d oral IMI in terms of antidepressive efficacy, but significantly better tolerated. These findings suggest interesting perspectives for the use of SAMe in depression.

Adolescent↗
PubMed1994

Surface ionization organic mass spectrometry of imipramine, desipramine, clomipramine, and lidocaine.

Surface ionization organic mass spectrometry (SIOMS) has been performed on some clinically important drugs (imipramine, desipramine, clomipramine, lidocaine) by using quadrupole mass spectroscopy in which the thermal ion source has a rhenium oxide emitter. The mass spectra were presented, interpreted in a purely empirical way, by means of evidence from previous investigations, and then compared to conventional EI techniques. Sensitivity and selectivity have also been studied, demonstrating that (a) these drug compounds are efficiently surface-ionized, (b) experimental results rationalize the high sensitivity of the surface ionization detector (SID) of gas chromatography (GC) for the examined drugs, and (c) the GC/SIOMS coupling can be used for sensitive and selective detection of the drugs in the serum. An approach to detection of these drugs in serum by GC/SIOMS and GC with SID is described. The characteristics of both methods provide a reliable, sensitive, and selective method, which is needed for low concentration level measurements in complex mixtures.

Clomipramine↗
PubMed2004

Effects of antidepressant drug imipramine on gene expression in rat prefrontal cortex.

We have investigated gene expression changes produced by acute and chronic daily treatment with a prototypical antidepressant, imipramine, using DNA microarrays. The analysis of similarities in gene expression patterns among functionally related genes revealed four expression profile cluster areas that showed a highly significant overrepresentation of several functional classes. Genes encoding for proteins involved in cAMP metabolism, postsynaptic membrane proteins, and proto-oncogenes were overrepresented in different cluster areas. Furthermore, we found that serine proteases as a group were similarly regulated by chronic antidepressant treatment. Our data suggest that cAMP metabolism, synaptic function, and protein processing by serine proteases may be important targets of antidepressant treatment and potential objects for antidepressant drug development.

Algorithms↗
PubMed1982

Active metabolites of imipramine and desipramine in man.

Active hydroxy metabolites of imipramine (IMI) and desipramine (DMI) have been quantified in plasma and cerebrospinal fluid (CSF) from patients at steady-state. In plasma of prepubescent boys and adults the concentration of unconjugated 2-hydroxyimipramine is only 15% to 25% that of IMI; 2-hydroxydesipramine (OH-DMI) concentration, however, is usually 50% that of DMI and in some cases OH-DMI is the predominant compound. In CSF from adult patients the ratio of concentrations of OH-DMI/DMI is higher than in plasma. Judging from the CSF/plasma ratio 12% of DMI exists in the free form at steady state, whereas 16% of OH-DMI is free (P less than 0.02). There is no evidence for saturation of hydroxylation within the therapeutic dose and concentration ranges investigated. On the basis of a steady-state OH-DMI/DMI ratio of less than 1/30 in plasma 5% of the population studied could be classified as deficient DMI hydroxylators. This in the same as the incidence of deficient debrisoquine hydroxylators reported in other populations.

Adolescent↗
PubMed1985

Effects of amitriptyline and imipramine on brain amine neurotransmitter metabolites in cerebrospinal fluid.

The effects of amitriptyline (AMI) or imipramine (IMI) on levels of 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA) (the major brain metabolites of the neurotransmitters norepinephrine [NE], serotonin [5-HT], and dopamine [DA]) in cerebrospinal fluid were determined in 66 subjects with unipolar and bipolar depression. There were significant reductions in MHPG and 5-HIAA levels for the depressed group taken as a whole, but levels of HVA did not change significantly. The changes were similar when subjects were grouped as treated with AMI and IMI and with unipolar and bipolar depression. Reductions in MHPG and 5-HIAA levels were greater in women than in men. In all subjects with depression and in those treated with AMI and IMI, amine metabolite changes did not differ significantly between those who had a positive clinical response to drug therapy and those who did not. Responders with bipolar depression had smaller reductions in MHPG levels than did responders with unipolar depression. The similar effects of AMI and IMI on MHPG and 5-HIAA differ from the dissimilar effects of the two drugs on NE and 5-HT amine uptake systems reported in animal and in in vitro studies. Results provide conclusive evidence of the effects of AMI and IMI on noradrenergic and serotonergic (but not dopaminergic) systems in patients with depression.

Adult↗
PubMed1986

Targeting imipramine dose in children with depression.

The response to imipramine (IMI) in children with depression has been shown to correlate with total levels of IMI plus its active metabolite desmethylimipramine (DMI). The pharmacokinetics of IMI + DMI in children with depression are examined, and the single-point prediction of steady-state IMI + DMI levels at minimum therapeutic concentrations for prepubertal depression is proposed. With a single, 25 mg oral dose of IMI, a plasma concentration of IMI + DMI 24 hours after dosing correlates (r = 0.92) with steady-state IMI + DMI levels in children with depression receiving 3 mg/kg/day IMI. The targeting of IMI dose in the child population with depression to rapidly achieve a minimum therapeutic concentration is shown to be feasible and reliable within theoretic limits.

Absorption↗
PubMed1998

Influence of various combinations of specific antibody dose and affinity on tissue imipramine redistribution.

1. This study was designed to evaluate the distribution kinetics of imipramine (Imip) in the brain and the main peripheral organs (heart, kidney, liver and lung) of rats, and to establish the relationship between the redistribution of Imip from these tissues and the immunoreactive capacity (dose and affinity) of anti-TCA IgG. 2. [3H]-Imip (1 nmol kg(-1) body weight) was injected intravenously 6 min before the i.v. injection of antibodies. At this time, the concentrations of Imip and its main metabolites in plasma were determined. The radioactivity measured corresponded to 91.7% Imip, indicating that the pharmacokinetics reflected essentially Imip. Plasma and tissue Imip contents were measured over the interval 1 to 90 min in control and in treated rats. The antibodies used were a murine monoclonal IgG1 (Ka=3.8 10(7) M(-1)) at an IgG1/Imip molar ratio of 1000 (IgG1 1000), and a sheep polyclonal IgG (TAb, Ka=1.3 10(10) M(-1)) at IgG/ Imip molar ratios of 1, 10 and 100 (TAb1, TAb10 and TAb100). 3. The anti-TCA IgG increased the plasma [3H]-Imip concentrations: the AUC1-->60 min for [3H]-Imip were 4 (IgG1 1000), 9 (TAb1), 33.9 (TAb10) and 41.4 (TAb100) times higher in the treated groups than in the controls. The opposite effect occurred in the brain, heart and lungs, with large, rapid decreases in Imip. The increase in plasma Imip and the decrease in tissue Imip depended on the immunoreactive capacity (NKa) of the antibody, where N=molar concentration of IgG binding sites and Ka=IgG affinity constant. Maximal plasma and tissue redistribution occurred when NKa=33.8 x 10(4). 4. Imip redistribution can be controlled using various doses or affinities of specific antibodies, and the resulting rapid, extensive Imip redistribution from the main target organs could be very promising for TCA detoxification.

Animals↗
PubMed2005

The antidepressant imipramine inhibits M current by activating a phosphatidylinositol 4,5-bisphosphate (PIP2)-dependent pathway in rat sympathetic neurones.

Little is known about the intracellular actions of imipramine (IMI) in the regulation of ion channels. We tested the action of IMI on the intracellular cascade that regulates M current (I(M)) in superior cervical ganglion neurones (SCGs). Dialysis of the cells with GDPbetaS, a G protein signaling blocker, did not disrupt the inhibition of I(M). When we incubated the cells with the phospholipase C (PLC) inhibitor U73122, it prevented the I(M) inhibition by IMI. Also, when we dialyzed the cells with an intracellular Ca2+ chelator, it did not disrupt I(M) inhibition by IMI, as occurs in the M1 cascade. When we incubated the cells with the generic kinase inhibitor wortmannin, it prevented the recovery of I(M) from the inhibition by IMI. Also, when we applied phosphatidylinositol 4,5-bisphosphate (PIP2) intracellularly, it diminished the inhibition of I(M) by IMI. Our findings suggest that PLC is the target for IMI, that recovery of I(M) needs lipid phosphorylation for PIP2 resynthesis, and that IMI inhibits I(M) by activating a PLC-dependent pathway, likely by decreasing the concentration of PIP2.

Animals↗
PubMed2004

St John's wort and imipramine-induced gene expression profiles identify cellular functions relevant to antidepressant action and novel pharmacogenetic candidates for the phenotype of antidepressant treatment response.

Both the prototypic tricyclic antidepressant imipramine (IMI) and the herbal product St John's wort (SJW) can be effective in the treatment of major depressive disorder. We studied hypothalamic gene expression in rats treated with SJW or IMI to test the hypothesis that chronic antidepressant treatment by various classes of drugs results in shared patterns of gene expression that may underlie their therapeutic effects. Individual hypothalami were hybridized to individual Affymetrix chips; we studied three arrays per group treatment. We constructed 95% confidence intervals for expression fold change for genes present in at least one treatment condition and we considered genes to be differentially expressed if they had a confidence interval excluding 1 (or -1) and had absolute difference in expression value of 10 or greater. SJW treatment differentially regulated 66 genes and expression sequence tags (ESTs) and IMI treatment differentially regulated 74 genes and ESTs. We found six common transcripts in response to both treatments. The likelihood of this occurring by chance is 1.14 x 10(-23). These transcripts are relevant to two molecular machines, namely the ribosomes and microtubules, and one cellular organelle, the mitochondria. Both treatments also affected different genes that are part of the same cell function processes, such as glycolytic pathways and synaptic function. We identified single-nucleotide polymorphisms in the human orthologs of genes regulated both treatments, as those genes may be novel candidates for pharmacogenetic studies. Our data support the hypothesis that chronic antidepressant treatment by drugs of various classes may result in a common, final pathway of changes in gene expression in a discrete brain region.

Antidepressive Agents↗
PubMed1997

Effect of troleandomycin on the pharmacokinetics of imipramine in Chinese: the role of CYP3A.

AIMS: In vitro data indicate that imipramine (IMI), a widely used tricyclic antidepressant drug, is N-demethylated by several isoforms of cytochrome P450, which include CYP3A4. The aim of this study was to investigate the role of CYP3A in the in vivo N-demethylation of IMI. METHODS: Healthy subjects were given troleandomycin (TAO), a selective inhibitor of CYP3A, 250 mg daily for 2 days before a single oral dose of 100 mg IMI was administered. RESULTS: Pretreatment with TAO significantly increased the AUC of IMI by 59% (1971 +/- 938 vs 3134 +/- 2000 microg l(-1) h, 95% confidence interval for difference between means: 218 to 2108 microg l(-1) h, P < 0.05) and decreased its oral clearance by 30% (60.9 +/- 27.4 vs 42.5 +/- 22.7 l h(-1), 95% confidence internal for difference between means: 7.2 to 31.7 l h(-1), P < 0.05). CONCLUSIONS: We conclude that CYP3A may play an important role in the in vivo N-demethylation of IMI.

Adult↗
PubMed1997

Suppression of the rat micturition reflex by imipramine.

1. This study investigates possible mechanisms through which imipramine (IMI) exerts its antienuretic effect. The micturition reflex in response to bladder distension produced by saline infusion was examined in anaesthetized rats. 2. The amplitude and frequency of micturition reflex contractions were reduced by peripheral administration of IMI, but the micturition reflex was abolished after its intracerebroventricular (i.c.v.) administration. A muscarinic antagonist, atropine, displayed an inhibitory effect similar to that of IMI. A muscarinic agonist, carbachol, produced a dose-related rightward shift of the dose-response curve to IMI. Both IMI i.c.v. and the muscarinic antagonist l-methylscopolamine i.c.v. elevated the threshold of volume and pressure for micturition initiation, indicating that IMI and muscarinic antagonists mainly exert a central inhibitory effect on the micturition reflex. 3. In addition, to evaluate the role of central monoaminergic neurotransmission on micturition, the acetylcholine depletor hemicholinium-3 (HC-3), the catecholamines depletor alpha-methyl-p-tyrosine (AMPT), and the serotonin depletor p-chlorophenylalanine (PCPA) were examined alone or in combination with IMI. The micturition threshold was increased by treatment with HC-3, but not by AMPT or PCPA. In HC-3 treated rats, the inhibitory effect of IMI on the micturition reflex was more prolonged than in normal rats. After administration of IMI, the recovery from the cessation of micturition reflex contractions was facilitated by carbachol in normal rats, but not in HC-3 treated rats. This indicates that acetylcholine plays a facilitatory role in initiating micturition reflex contractions. 4. Acute treatment with IMI decreased the frequency and increased the volume threshold of micturition reflex contraction. Acute and chronic treatment with IMI prolonged the cessation period of micturition by IMI. 5. These results suggest that IMI exerts an inhibitory action on the micturition reflex by a central cholinergic mechanism. Muscarinic receptors located at the supraspinal level are tonically stimulated during distension-induced micturition reflex.

Adrenergic Uptake Inhibitors↗

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