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Tofranil (Imipramine)

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Generic Tofranil is a member of the family of drugs called tricyclic antidepressants. Generic Tofranil is used to treat depression. Generic Tofranil is also used on a short-term basis, along with behavioral therapies, to treat bed-wetting in children aged 6 and older. Sometimes Generic Tofranil is prescribed to treat bulimia, attention deficit disorder in children, obsessive-compulsive disorder and panic disorder.

Other names for this medication:

Similar Products:
Pamelor, Norpramin, Silenor, Zonalon, Aventyl, Norpress, Elavil


Also known as:  Imipramine.


Generic Tofranil is used to treat depression. Generic Tofranil is also used on a short-term basis, along with behavioral therapies, to treat bed-wetting in children aged 6 and older. Sometimes Generic Tofranil is prescribed to treat bulimia, attention deficit disorder in children, obsessive-compulsive disorder and panic disorder.

Generic Tofranil is a member of the family of drugs called tricyclic antidepressants.

Tofranil is also known as Imipramine, Antideprin, Deprenil, Deprimin, Deprinol, Depsonil, Dynaprin, Eupramin, Imipramil, Irmin, Janimine, Melipramin, Surplix, Antidep, Apo-Imipramine, Chrytemin, Daypress, Depsol, Ethipramine, Fronil, Imidol, Imimine, Imine, Imiprex, Imiprin, Impril, Medipramine, Melipramine, Mipralin, Novopramine, Primonil, Pryleugan, Sermonil, Sipramine, Talpramin, Tofnil, Tofranil-PM, Venefon.

Generic name of Generic Tofranil is Imipramine hydrochloride.

Brand names of Generic Tofranil are Tofranil, Tofranil-PM.


Take Generic Tofranil orally.

Take Generic Tofranil with or without food.

For adults

The usual starting dose is 75 mg a day. The maximum daily dose is 200 mg.

For children

Total daily dosages for children should not exceed 2.5 mg for each 2.2 pounds of the child's weight. Doses usually begin at 25 mg per day. This amount should be taken an hour before bedtime. If needed, this dose may be increased after 1 week to 50 mg (ages 6 through 11) or 75 mg (ages 12 and up), taken in one dose at bedtime or divided into 2 doses, 1 taken at mid-afternoon and 1 at bedtime.

Aged people

The usual dosage should start with 25 to 50 mg per day. The dose may be increased as necessary, but effective dosages usually do not exceed 100 mg a day.

If you want to achieve most effective results do not stop taking Generic Tofranil suddenly.


If you overdose Generic Tofranil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Tofranil overdosage: agitation, bluish skin, convulsions, difficulty breathing, dilated pupils, drowsiness, heart failure, high fever, involuntary writhing or jerky movements, irregular or rapid heartbeat, lack of coordination, low blood pressure, overactive reflexes, restlessness, rigid muscles, shock, stupor, sweating, vomiting.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Tofranil are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Tofranil if you are allergic to Generic Tofranil components.

Be very careful with Generic Tofranil if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not take Generic Tofranil if you are recovering from a recent heart attack or take MAO inhibitors, such as the antidepressants Nardil and Parnate.

Be very careful with Generic Tofranil if you have diabetes, hypoglycemia, a history of mental disorders.

Be very careful with Generic Tofranil if you are taking albuterol (Proventil, Ventolin), antidepressants that act on serotonin, including Prozac, Paxil and Zoloft, antipsychotic drugs such as Mellaril and chlorpromazine, barbiturates such as Nembutal and Seconal, blood pressure medications such as Catapres, Carbamazepine (Tegretol), cimetidine (Tagamet), decongestants such as Sudafed, drugs that control spasms, such as Cogentin, Epinephrine (EpiPen), Flecainide (Tambocor), Guanethidine, Methylphenidate (Ritalin), Norepinephrine, other antidepressants such as Elavil and Pamelor, Phenytoin (Dilantin), Propafenone (Rythmol), Quinidine, thyroid medications such as Synthroid, tranquilizers and sleep aids such as Halcion, Xanax, and Valium.

Avoid alcohol.

Do not participate in any activities that require full alertness if you are unsure about your ability.

Try to stay out of the sun as much as possible.

It can be dangerous to stop Generic Tofranil taking suddenly.

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Accumulating data links inflammation, oxidative stress and immune system in the pathophysiology of major depressive disorders. Sickness behaviour is a set of behavioural changes that develop during infection, eventually leading to decrease in mobility and depressed behaviour. Lipopolysaccharide (LPS) induces a depression-like state in animals that mimics sickness behaviour. Caffeic acid, a naturally occurring polyphenol, possesses antioxidant and anti-inflammatory properties. The present study was designed to explore the potential of caffeic acid against LPS-induced sickness behaviour in mice. Caffeic acid (30mg/kg) and imipramine (15mg/kg) were administered orally one hour prior to LPS (1.5mg/kg) challenge. Behavioural assessment was carried out between 1 and 2h and blood samples were collected at 3h post-LPS injection. Additionally, cytokines (brain and serum) and brain oxidative stress markers were estimated. LPS increased the systemic and brain cytokine levels, altered the anti-oxidant defence and produced key signs of sickness behaviour in animals. Caffeic acid treatment significantly reduced the LPS-induced changes, including reduced expression of inflammatory markers in serum and whole brain. Caffeic acid also exerted an anti-oxidant effect, which was evident from the decreased levels of oxidative stress markers in whole brain. Our data suggests that caffeic acid can prevent the neuroinflammation-induced acute and probably the long term neurodegenerative changes.

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Help-seeking behaviour for treatment of panic disorder was investigated in the sample of the Cross-National Collaborative Panic Study Second Phase. A total of 1168 patients were entered into this trial in 14 countries. Although there were significant center differences in prior treatment and utilization of health services there were also similarities. Treatment had been provided mainly by general practitioners. Drug treatment consisted mostly of prescription of classical tranquilizers and had a longer duration than treatment by psychotherapy. Patients with agoraphobic avoidance, past major depression and longer duration of illness used medical and psychiatric treatment facilities more intensely. Older and more severely disabled subjects were more frequently treated by medical health care providers and were more likely to receive psychotropic drugs. The results indicate that general practitioners carry an important load in the treatment of panic disorders but may need more information about recent development in pharmacotherapy for this condition.

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Ten patients with psychotic depression were assessed on a battery of clinical, EEG, psychological, and biochemical measures during treatment with imipramine (150 mg/day). Significant changes occurred in the scores on self-rated and observer-rated depression scales and on an observer-rated side effect scale. Significant changes also occurred in the EEG evoked response, but the effects on spontaneous activity were minimal. The psychological measures revealed an improvement in performance as treatment progressed. The clinical significance of the changes observed was assessed with reference to their correlations with the clinical rating scores and with the plasma concentrations of imipramine and desmethylimipramine, and the changes observed following the administration of imipramine to non-depressed normal subjects. Changes in evoked EEG activity seemed on balance to be direct central effects of imipramine, whereas changes in psychological performance appeared to be secondary to clinical change.

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A rapid and sensitive ultraperformance liquid chromatography tandem mass spectrometry assay was developed for the simultaneous analysis of oxcarbazepine and its main metabolite in human plasma. The assay involves a simple solid-phase extraction procedure of 0.3 mL of human plasma and analysis was performed on a triple-quadrupole tandem mass spectrometer in multiple reaction monitoring mode via electrospray ionization. Separation was achieved on an Acquity UPLC™ BEH C₁₈ column (50 × 2.1 mm, i.d., 1.7 µm) with isocratic elution at a flow-rate of 0.25 mL/min and imipramine was used as the internal standard. The standard calibration curve was linear over the range 9.580-5070.205 ng/mL for oxcarbazepine (OXC) and 19.444-10290.800 ng/mL for 10,11-dihydro-10-hydroxycarbamazepine (MHD), expressed by the linear correlation coefficient r², which was better than 0.995 for OXC and MHD. The intra- and inter-day precision and accuracy of the quality control samples were within 10.0%. The recoveries were 81.0, 89.6 and 66.6% for OXC, MHD and imipramine, respectively. The total run time was 1.5 min only for each sample, which makes it possible to analyze more than 350 samples per day.

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Repeated oral administration of 20 mg/kg imipramine elevated the level of 5-HT2C mRNA in the rat brain. Hybridization signals in nearly all regions stained by digoxigenin-labeled antisense cRNA probe, such as the hippocampus, choroid plexus, habenular nucleus, and dorsomedial hypothalamic nucleus, were more intense following imipramine treatment. These results suggest that long-term treatment with imipramine stimulates 5-HT2C receptor gene expression.

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Local rates of cerebral glucose metabolism were determined in four groups of adult rats 4 weeks after surgery: sham-operation + saline; thyro-parathyroidectomy (TX) + saline; sham-operation + imipramine; or TX + imipramine. Daily i.p. injections, imipramine at 10 mg/kg or saline at 1 ml/kg b.w., were given during the 2 weeks before the deoxyglucose experiment. TX reduced glucose utilization in the limbic, motor, endocrine and auditory systems. Imipramine reduced glucose metabolism in the median eminence, both habenular nuclei and several limbic regions including the amygdala, hippocampus and parietal cortex. Five structures showed significant interactions between TX and imipramine. In three of these regions, the supraoptic nucleus, central amygdala and lateral habenula; TX and/or imipramine individually reduced metabolism and the combined treatment raised it back to within the normal range. In the dorsal raphe, TX and imipramine tended to increase metabolism and the combined treatment resulted in a decrease to within normal range. The neurohypophysis, unaffected by TX alone, showed a significant increase in activity when TX was combined with imipramine. These data indicate, in part, that both hypothyroidism and imipramine treatment alone depress metabolism in limbic forebrain and the major limbic-brainstem relay nuclei. Combined treatment normalizes metabolism in many of these limbic pathways. Hypothetically, hypothyroidism may alter central catecholamine function in such a way that the metabolic response to imipramine is reversed or altered.

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Interaction of Chlorpromazine with tricyclic antidepressants was investigated in twenty schizophrenic patients after their concurrent administration. A significant increase in serum chlorpromazine concentration was observed when administered in combination with both amitriptyline and imipramine with chlorpromazine. If combined therapy is indicated, the dose of chlorpromazine should be reduced or the time of administration of other two drugs should be adjusted to maintain therapeutic levels of chlorpromazine.

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Nocturnal enuresis is a common childhood disorder. Tricyclic antidepressants and anticholinergic agents have been the well accepted pharmacological treatment for this disorder and are efficacious in 40-70% and 10-50% of cases, respectively. The present study was performed to evaluate the effect of a combined treatment of tricyclic antidepressant and an anticholinergic agent. Twenty-two children aged 6-12 years with primary monosymptomatic nocturnal enuresis who did not prefer to use a conditioning alarm were given a combined treatment of these drugs. After a control period of 1 month, each patient was treated for 6 months and then observed for 3 months. A 30-mg dose of amitriptyline or imipramine was given with either 2-4 mg oxybutinin or 10-20 mg propiverine. Efficacy was determined relative to the number of wet nights per week compared with the control period, with more than a 50% decrease in wet nights per week taken to indicate efficacy. The mean wet nights per week decreased from 6.1 to 1.7 (P<0.01), and efficacy was established in 20 patients (90.9%). Relapses occurred in 60.0% of patients during the follow-up period. No significant side effects were observed. The efficacy of the combined therapy in monosymptomatic nocturnal enuresis appears to be greater than that reported for either drug alone, and therefore can be a choice of treatment in order to motivate children with nocturnal enuresis.

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Two transport systems for serotonin were measured independently in osmotic lysates of porcine platelets. After pre-equilibration with potassium phosphate and dilution into NaCl medium, only the plasma membrane transport system was observed. Under these conditions, serotonin accumulation is inhibited by imipramine, but not by reserpine or norepinephrine, and requires high (100 meq/liter) concentrations of Na+. In the presence of ATP at low (10 meq/liter) concentrations of Na+, only the transport system of the intracellular serotonin storage organelles was observed. Under these conditions, transport is inhibited by reserpine, norepinephrine, and epinephrine, but not by imipramine, and requires either ATP or an artificially imposed pH gradient (interior acidic) across the organelle membrane. These and other results suggest that accumulation of serotonin in platelet storage organelles is coupled predominantly to the pH gradient across the membrane.

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It has been established that thyrotropin-releasing hormone (TRH) affects several aspects of immunoreactivity, e.g. production of proinflammatory cytokines. It has been shown that TRH enhances the therapeutic efficiency of classical tricyclic antidepressants. Proinflammatory cytokines may play a role in the etiology of depression, whereas the therapeutic efficacy of antidepressants may be related to their negative immunoregulatory effects.

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The composition of excipients necessary to produce tablets comprising imipramine and magnesium was established. All of prepared tablets were in compliance with the pharmacopoeial requirements. The release tests showed that above 80% of imipramine was released within 20-35 min and 80-76% of magnesium up to 45 min from the composed tablets and one-ingredient tablets, respectively.

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A liquid chromatographic (LC) procedure has been developed for the assay, content uniformity, and identification of single active ingredient solid and liquid formulations of amitriptyline, chlorpromazine, imipramine, thioridazine, and trifluoperazine. The drugs are extracted from their formulations with methanol or dilute hydrochloric acid, and identified by comparison of retention times with those of known standards; drugs are quantitated against these standards with dl-norephedrine hydrochloride as the internal standard. The precision of replicate injections is better than 2.5% for peak area and better than 1% for peak height. The precision of triplicate determinations of tablet composites is better than 2.2%.

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The aim of this review is to assess the effectiveness of such drugs in aiding long term smoking cessation. The drugs include bupropion; buspirone; diazepam; doxepin; fluoxetine; imipramine; meprobamate; moclobemide; nortriptyline; tryptophan; ondansetron; venlafaxine and the beta-blockers metoprolol, oxprenolol and propanolol.

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Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) are synthesized by adenylate cyclase and guanylyl cyclase and degraded by phosphodiesterases. Antidepressant treatment action is hypothesized to occur through increased cAMP signaling; however, antidepressants are also reported to increase phosphodiesterase-4 expression. We addressed this paradox by systematically studying elements of intracellular signaling in the hippocampus of rats chronically treated with imipramine. We observed decreases in cAMP levels, which were congruent with our findings of increased gene expression for phosphodiesterases and decreased adenylate cyclase. Immunoassay results showed unchanged cGMP and brain-derived neurotrophic factor levels. We conclude that in contrast with the assumption of antidepressant-mediated increases in cAMP levels, longterm imipramine treatment may have the opposite effect, namely decreased hippocampal cAMP.

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Tricyclic antidepressants (TADs) are known to antagonize the hypotensive and sedative actions of clonidine. We compared the effects of bupropion and imipramine pretreatment on the acute hypotensive and sedative actions of clonidine in eight normotensive male subjects in a randomized, double-blind crossover study. Pretreatment with bupropion, 100 mg by mouth three times a day for 9 days, had no effect on baseline supine blood pressure (BP) and heart rate (HR) and did not modify the hypotensive, bradycardic, and sedative actions of clonidine. Imipramine, 25 mg by mouth three times a day for 9 days, increased supine and standing HR and decreased standing systolic BP. In half the subjects the hypotensive action of clonidine was reduced 40% to 50% by imipramine. The specific binding of 3H-yohimbine to alpha 2-receptors of platelet membranes was not affected by pretreatment with either antidepressant. In spontaneously hypertensive rats, 16 days of bupropion, 25 mg/kg subcutaneously, had no effect on baseline BP and HR and did not antagonize the hypotensive and bradycardic effects of clonidine, 5 mg/kg iv. Pretreatment with desipramine, 5 mg/kg subcutaneously for 16 days, accelerated baseline HR and reduced cardiovascular actions of clonidine. These observations suggest that not all antidepressants antagonize the effects of clonidine. If the negative interaction between TADs and clonidine is a result of sensitivity of alpha 2-receptors, these receptor changes are not the common denominator of antidepressant activity and may only be seen with TADs.

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Enuresis (bedwetting) is a socially disruptive and stressful condition which affects around 15-20% of five year olds, and up to 2% of young adults. Although there is a high rate of spontaneous remission, the social, emotional and psychological costs to the children can be great.

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The past decade has witnessed a sustained search for an effective pharmacotherapeutic agent for the treatment of cocaine dependence. While administration of cocaine acutely increases intercellular dopamine, serotonin, and norepinephrine levels by blocking their presynaptic reuptake, chronic cocaine abuse leads to down-regulation of monoamine systems. Post-cocaine use depression and cocaine craving may be linked to this down-regulation. Antidepressant pharmacotherapy, by augmenting monoamine levels, may alleviate cocaine abstinence symptomatology, as well as relieving dysphoria and associated craving by general antidepressant action.

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Specific binding of [3H]imipramine and [3H]paroxetine was simultaneously examined in human brains (frontal cortex, temporal cortex, cingulate cortex, hypothalamus, hippocampus and amygdala) from 11 controls and 11 depressed suicide victims. A single saturable high affinity site was obtained for both radioligands. Age was not related to significant changes in [3H]imipramine and [3H]paroxetine binding parameters, which indicates the stability of the brain serotonergic system with increasing age. A major finding of the present study concerns the existence of a significant decrease in the maximum number (Bmax) of [3H]imipramine binding sites in hippocampus from depressed suicides as compared with the control group, without changes in the binding affinity (Kd). In contrast, when [3H]paroxetine was used as radioligand, no changes in either Bmax or Kd were detected in any of the brain regions studied. These findings suggest that [3H]imipramine may be a better marker than [3H]paroxetine when alterations in the presynaptic serotonergic uptake site are to be detected.

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Imipramine hydrochloride (CAS 113-52-0) is a widely used antidepressant and can interact with opioid receptors. However, complete information concerning possible regional alterations in mu-opioid receptor expression in the rat forebrain after chronic treatment with this substance is still lacking. This being the case, analysis of mu-opioid receptor immunostaining in several regions of the rat brain after imipramine administration in vivo was made, and an increase in the density of cells expressing mu-opioid receptors in the caudatus-putamen, the dentate gyrus and the frontal, parietal and piriform cortices after chronic imipramine treatment, with respect to controls, was found. These data suggest that mu-opioid receptor expression in the rat forebrain is altered by in vivo chronic imipramine treatment.

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On plain X-ray films of the spine, spina bifida occulta (lumbar vertebrae in three, lumbosacral vertebrae in 19 and sacral vertebrae in 31) was recognized in 53 children (69%). Ultrasonographic bladder abnormalities were recognized in 40 children (52%). Children with lumbar and lumbosacral spina bifida occulta showed a higher rate of concomitant ultrasonographic bladder abnormalities (P = 0.006) and had a poorer response to treatment (P = 0.041) compared with the children who had sacral spina bifida occulta. Children with ultrasonographic bladder abnormalities had a worse response to treatment (P = 0.005) compared to the children without bladder abnormalities.

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CPAE cells demonstrated a time-dependent increase in 123I-MIBG uptake that reached a relative plateau (mean +/- SD) at 4 h of 375.6% +/- 5.9% the 30-min level. When the culture medium was changed after 30 min of uptake, 123I-MIBG gradually was eluted from the cells at an efflux rate of 43.8% over 2 h. Western blotting confirmed the presence of NE transporters in CPAE cells. The uptake 1 inhibitors desipramine, imipramine, and phenoxybenzamine at 50 micromol/L reduced 123I-MIBG uptake to 55.3% +/- 2.7%, 62.4% +/- 3.5%, and 48.0% +/- 2.2% control levels, respectively, whereas none of the uptake 2 inhibitors had an effect. Exposure to hypoxia resulted in a reduction in 123I-MIBG uptake to 77.5% +/- 0.2% and 50.0% +/- 3.4% control levels at 0.5 and 4 h, respectively. PMA (10 ng/mL) and L-NAME (2 nmol/L) decreased 123I-MIBG uptake to 76.7% +/- 9.0% and 86.5% +/- 5.6% control levels, respectively.

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Noxious stimulation can suppress epileptic seizures in humans and epileptiform activity in laboratory animals. Using as a model system the focal epileptiform activity (FEA) induced by the pneumophoresis of penicillin, the role of 5-hydroxytryptamine (5HT) in suppression of this activity by noxious stimulation was investigated. Drugs known to depress dorsal raphe unit activity, (+/-)-8-hydroxydipropylaminotetralin (DPAT), imipramine, and fluoxetine prevented suppression of FEA induced by noxious stimulation. Desimipramine, which depresses locus ceruleus but not dorsal raphe unit activity, was ineffective in blocking the suppression. Quipazine, an agonist at 5-HT receptors, in part restored the suppression that had been blocked by DPAT or imipramine. Several serotonin antagonists effective at 5-HT1 and 5-HT2 receptors blocked suppression, but an unequivocal determination of the serotonin receptor subtype mediating suppression could not be made. We conclude that 5-HT mediates suppression of FEA induced by noxious stimulation.

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These results suggest that delusional depressions might have a different neurobiological substrate with loss of chronobiological rhythms.

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To assess the effects of drugs other than desmopressin and tricyclics on nocturnal enuresis in children, and to compare them with other interventions.

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The effects of acute and repeated administration of S 20098 were compared with those of melatonin (4, 8, 16, 32, 64 mg/kg intraperitoneally [IP] for mice), imipramine (64 mg/kg orally for rats, 8 mg/kg IP for mice) and fluoxetine (16 mg/kg IP for mice). The influence of the pretreatments with 5-HT(1A) or 5-HT(1B) receptor agonists (8-OH-DPAT, anpirtoline) and 5-HT(1A/1B), 5-HT(2A/2C) or 5-HT(3) antagonists (pindolol, ritanserin, ondansetron) on the effects of S 20098 or melatonin were compared with imipramine and fluoxetine in mice.

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This study examines retrospectively the response rate of pediatric burn survivors with acute stress disorder to either imipramine or fluoxetine.

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tofranil drug interactions 2015-06-25

A simultaneous assay for imipramine, desipramine and their 2- and 10-hydroxy-metabolites using high-performance liquid chromatography (HPLC) is described. The drugs and internal standard, pericyazine, were extracted from plasma or urine at pH 9. buy tofranil 6 with diethyl ether and back-extracted into 0.1 M orthophosphoric acid. The recovery of the compounds ranged from 78.6% for imipramine to 94.3% for 2-hydroxydesipramine. The extracts were analysed by reversed-phase HPLC with electrochemical detection using a mobile phase of 30% acetonitrile in 0.1 M K2HPO4 at pH 6.0 delivered at 2 ml/min. All compounds were resolved in a run time of 15 min with lower limits of quantification of 1.5 ng/ml for hydroxy-metabolites and 3 ng/ml for imipramine and desipramine. The intra- and inter-day coefficients of variation at 50 ng/ml were 5.2% and 6.8%, respectively (n=8).

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A rabbit liver UDP-glucuronosyltransferase cDNA that is related to human and rat UGT1A7 has been identified. The predicted amino acid sequence of the UGT1A71 displays 80% similarity to buy tofranil that encoded by human HP4 (UGT1A9), but 81% to that predicted for human UGT1A7 and 77% to the rat UGT1A7 (UGTA2). The exons encoding human UGT1A7 and rat UGTA2 are the seventh of the series of cassette exons that flank the 3' common exon series of the UGT1A locus. Southern blot analysis demonstrates that the exon sequence encoding UGT1A71 is part of a larger cluster of highly related genes. The UGT1A71 RNA is expressed in both neonatal and adult liver, and unlike rat UGT1A2 which is inducible with Ah receptor ligands such as polycyclic aromatic hydrocarbons, rabbit UGT1A7 is not regulated when animals are exposed to these inducers. Following expression of UGT171 in COS-1 cells, glucuronidation activity was identified for small phenolic molecules like 4-nitrophenyl, bulky phenols as represented by 4-hydroxybiphenol and octylgallate, as well as 4-hydroxyestrone. In addition, UGT1A71 possesses catalytic activity toward tertiary amines like the tricyclic antidepressant imipramine. The pattern of UGT1A71 glucuronidation is similar to that observed for human UGT1A9, except tertiary amines are not subject to glucuronidation by human UGT1A9. Glucuronidation of tertiary amines is catalyzed principally by human UGT1A4 as well as rabbit UGT1A4. Although rabbit UGT1A7 catalyzes the formation of quarternary ammonium glucuronides, the Vmax is considerably less than that observed for rabbit UGT1A4. Overall, the characterization of rabbit UGT1A7 suggests that this protein represents the ortholog of the human UGT1A7, which to date has not been identified.

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Addition of human cerebrospinal fluid (CSF) induced a marked inhibition of 3H-paroxetine binding to the monkey cortical membranes, while the specific binding of 3H-imipramine was slightly inhibited. Moreover, 3H-serotonin (5-hydroxy-tryptamine, 5-HT) uptake inhibition in the monkey cortical synaptosomes was also increased as the volume of added CSF was increased. Scatchard analysis of specific 3H-paroxetine binding with human CSF showed non-competitive kinetics, although CSF was competitive with 3H-imipramine binding. The inhibitory effect of human CSF on 5-HT uptake was non-competitive in nature. The endogenous buy tofranil substances in human CSF most probably act at the recognition site labeled with 3H-paroxetine. Moreover, occupation of this site by the endogenous substances is likely to inhibit the 5-HT uptake process.

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The Bmax and Kd values for [3H]imipramine binding were measured in platelets from drug-free normal controls and schizophrenic and depressive patients. No differences among groups were found. Exacerbated and remitted patients with either schizophrenia or depression did not differ in platelet [3H]imipramine binding parameters. No correlations were observed between platelet [3H]imipramine binding parameters and measures of symptom severity among actively ill patients buy tofranil with either schizophrenia or depression.

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It has been suggested that increased platelet activation increases the risk of acute myocardial infarction (AMI) in patients with depression. buy tofranil Selective serotonin reuptake inhibitors (SSRIs) may attenuate platelet activation by serotonin depletion in platelets. Observational studies have shown discrepant results of AMI risk associated with the use of SSRIs.

tofranil overdose death 2015-05-07

Physical activity and antidepressant treatment have each separately been of significant interest for the management of Alzheimer's disease (AD); particularly the behavioral problems associated with this dementing disorder. We have found that combined antidepressant treatment and physical activity have an additive, potentiating effect on BDNF mRNA expression within several areas of the rat hippocampus. During the 20-day experimental period, animals were treated daily with imipramine (15 mg/kg) or tranylcypromine (7.5 mg/kg) by intraperitoneal injection. Exercising rat groups were given access to running wheels for the duration of the experiment. BDNF mRNA levels were assessed in several cell groups of the hippocampus by in situ hybridization, using a [35S] labelled riboprobe complementary to the full-length BDNF sequence, and computer-assisted densitometry. The combination of physical buy tofranil activity and antidepressant treatment for the 20-day period led to a significant potentiation of full-length BDNF mRNA levels within the dentate gyrus and CA 1, CA 3, and CA 4 cellular fields, above the levels obtained with each intervention alone. These results provide impetus for the study of physical exercise as a potential enhancer of treatment response to antidepressants.

tofranil missed dose 2016-10-21

A study has been made of the action of the neuropeptide proctolin on the radiosodium efflux from single barnacle muscle fibers. Proctolin (10(-8) M) when applied externally causes stimulation of the Na efflux in unpoisoned and ouabain-poisoned fibers. The response is prompt in onset, reaches a peak in 15 min and decays slowly. The response of the ouabain-insensitive Na efflux to external proctolin is dose-dependent, the concentration threshold being less than 10(-10) M. The response to proctolin is dependent on external Ca2+ but not on Na+. (i) The response to proctolin is abolished by high external Mg2+, as well as by verapamil, Co2+, Cd2+ and WB-4101. (ii) The response buy tofranil is also abolished by preinjecting 0.5 M MgCl2 or 0.1 M EGTA. The calmodulin antagonists trifluoperazine and imipramine are without effect on the response to proctolin. (i) Adenylate cyclase agonists, e.g. forskolin, fail to augment the response to proctolin. (ii) Prior injection of the phosphodiesterase inhibitors 1-propyl-3-methyl-7-(5-hydroxyhexyl)-xanthine (PMX) or 1-isoamyl-3-isobutylxanthine (IAX) fails to augment the response to proctolin. (iii) Prior injection of protein kinase inhibitor is ineffective. The response to proctolin is significantly reduced in the presence of tyramine. Taken together, these results support the view that proctolin stimulates the ouabain-insensitive Na efflux by activating Ca2+ channels and that the cAMP-protein kinase system is not involved in this response.

tofranil y alcohol 2016-06-20

The usefulness of guanethidine N-oxide formation as a measure of cellular flavin-containing monooxygenase activity was assessed using the purified hog liver enzyme, rat liver microsomes and hepatocytes. The apparent Km and Vmax for this reaction in hepatocytes were 0.30 +/- 0.20 mM and 0.81 +/- 0.36 nmole per 10(6) cells min-1 respectively. The Km for the purified enzyme was 0.31 mM and the Vmax was 0.56 nmole per microgram enzyme min-1. 2-Diethylaminoethyl-2,2-diphenyl valerate (SKF-525A) at a concentration of 0.5 mM had no effect on guanethidine N-oxide formation by either rat liver microsomes or the purified enzyme. In contrast 2,4-dichloro-6-phenylphenoxyethylamine (DPEA) at the same concentration caused greater than a 100% increase in the microsomal production of guanethidine N-oxide. The tertiary amines imipramine, chloropromazine and methylpyrilene inhibited N-oxide formation by both hepatocytes and the buy tofranil purified enzyme. These data indicate that guanethidine N-oxide formation can be used as a measure of cellular flavin-containing monooxygenase activity.

tofranil diet pill 2017-10-13

Platelet-activating factor (PAF) is a mediator of pulmonary oedema in acute lung injury that increases vascular permeability within minutes, partly through activation of acid sphingomyelinase (ASM). Since caveolae are rich in sphingomyelin and caveolin-1, which block endothelial nitric oxide (NO) synthase (eNOS) by direct binding, we examined the relationship between ASM, caveolin-1 and eNOS activity in the regulation of vascular permeability by PAF. In caveolar fractions from pulmonary vascular endothelial cells (isolated from perfused rat lungs) the abundance of caveolin-1 and eNOS increased rapidly after PAF perfusion. PAF treatment decreased endothelial NO (eNO) formation as assessed by in situ fluorescence microscopy. Restoration of eNO levels with PAPA-NONOate ((Z)-1-[N-(3-ammoniopropyl)-N-(n-propyl)amino]diazen-1-ium-1,2-diolate) mitigated the PAF-induced oedema. PAF treatment increased the ASM activity in caveolar fractions and perfusion with ASM decreased eNO production. Pharmacological inhibition of the ASM pathway with imipramine, D609 or dexamethasone blocked the PAF-induced increase of caveolin-1 and eNOS in caveolae, and the decrease in eNO production and oedema formation. We conclude that PAF causes ASM-dependent enrichment of caveolin-1 in caveolae of endothelial cells, leading to decreased eNO production which contributes to pulmonary oedema formation. These findings suggest rapid reduction in eNO production as a novel mechanism in the buy tofranil regulation of vascular permeability.

tofranil 50 mg 2016-03-10

Alprazolam is an anti-anxiety drug shown to be effective in the treatment of depression. In this study, the effect of sympathetic receptor antagonists on alprazolam-induced antidepressant action was studied using a mouse model of forced swimming behavioral despair. The interaction of three sympathetic receptor antagonists with benzodiazepines, which may impact the clinical use of alprazolam, was also studied. Behavioral despair was examined in six groups of albino mice. Drugs were administered intraperitoneally. The control group received only a single dose of 1% Tween 80. The second group received a single dose of alprazolam, and the third group received an antagonist followed by alprazolam. The fourth group was treated with imipramine, and the fifth group received an antagonist followed by imipramine. The sixth group was treated with a single dose of an antagonist alone (atenolol, a β1-selective adrenoceptor antagonist; propranolol, a non selective β-adrenoceptor antagonist; and prazocin, an α1-adrenoceptor antagonist). Results confirmed the antidepressant action of alprazolam and imipramine. Prazocin treatment alone produced depression, but it significantly potentiated the antidepressant actions of imipramine and alprazolam. Atenolol alone produced an antidepressant effect and potentiated the antidepressant action of alprazolam. Propranolol treatment alone produced depression, and antagonized the effects of alprazolam and imipramine, even producing depression in buy tofranil combined treatments.In conclusion, our results reveal that alprazolam may produce antidepressant effects through the release of noradrenaline, which stimulates β2 receptors to produce an antidepressant action. Imipramine may act by activating β2 receptors by blocking or down-regulating β1 receptors.

tofranil 25mg medication 2017-05-31

3-Cyano-imipramine (cianopramine) is a potent and selective inhibitor of serotonin uptake into synaptosomes. In a double-blind trial, 60 patients with various types of depression fulfilling the DSM-III criteria of depressive episodes were treated with either cianopramine (n = 20, mean daily dose 3.3 +/- 0.6 mg) amitriptyline (n = 20, mean daily dose 86.4 +/- 21 mg) or placebo (n = 20) orally. According to the ratings of the Hamilton Scale of Depression and clinical global evaluations, both active drugs showed statistical superiority over placebo (P less than 0.02). The buy tofranil frequencies of anticholinergic side effects in the cianopramine group were comparable to those of the placebo group and were less than in the amitriptyline group. The findings suggest that cianopramine is a promising new antidepressant.

tofranil generic name 2016-10-15

Imipramine seems to be a better cost-utility antidepressant option for treating depressive disorders in primary care buy tofranil .

tofranil brand 2015-01-24

A case report of imipramine-induced syndrome of inappropriate antidiuretic hormone buy tofranil (SIADH) secretion in a 54-year-old woman is presented along with a review of the literature on antidepressant-induced SIADH. The clinical and laboratory presentation, diagnosis, treatment, and monitoring of antidepressant-induced SIADH also are discussed.

tofranil brand name 2015-06-10

Life stress was studied in relation to postrecovery attrition, symptom course, and recurrence of depression over 3 years. Participants were 67 individuals with recurrent depression who had responded to buy tofranil treatment. Life stress was assessed for the prior 12 weeks at acute treatment entry (T1), initial recovery (T2), and after 17 weeks of sustained recovery (T3). Severe life events at T1 predicted greater attrition, a more favorable postrecovery symptom course, and a lower likelihood of recurrence over 3 years. Life stress at T2 was not predictive of outcomes. Finally, undesirable life events at T3 tended to predict a worse symptom course and a higher likelihood of recurrence, particularly for individuals on medication. The findings are discussed in terms of (a) different processes influenced by life stress over time and (b) limitations of existing longitudinal research for studying the effects of life stress over prolonged intervals.

tofranil drug 2016-11-07

The functional capacity of guinea pig megakaryocytes was tested by studying their ability to concentrate serotonin and their response to agents which trigger the platelet release reaction. Megakaryocytes can concentrate 3H-serotonin as demonstrated by autoradiography after exposure to 0.5 muM 3H-serotonin and by quantitative measurement of isotope incorporation within 60 minutes. Uptake of isotope is rapid and linear within the first 30 minutes and tapers off between 30 and 60 minutes. Incorporation of isotope is diminished during exposure to cold, 2 muM reserpine, and 20 muM imiprimine. The following triggering agents: 10(-5) to 10(-3) M ADP, 1 to 100 units of thrombin, 10(-5) to 10(-3)M epinephrine, and 1 to 12 muM ionophore A23187 all produce significant release of stored 3H-serotonin. In the presence of ADP, albumin and serum completely inhibit the release of serotonin. Scanning microscopic studies show that coincident with serotonin release the triggering agents produce marked changes in cell shape. Transmission electron microscopy on these cells shows that there is the appearance of a prominent contraction zone, which is composed of microfilaments, and also variable diminution of cytoplasmic granules. The specifically induced serotonin release from megakaryocytes coupled with shape change and evidence of cell contraction produced by certain agents demonstrate one aspect of the functional Deltasone 10 Mg similarly between megakaryocytes and platelets.

recommended tofranil dosage 2017-05-07

Abnormal changes in platelets used as peripheral markers of Prograf Retail Cost central serotonergic functions are said to be associated with suicidality and depression, but this association has not been supported by consistent findings.

tofranil syrup 2016-09-18

Psychoactive drugs like chlorpromazine (CPZ), imipramine, lithium and amphetamine in one way or another affect behaviour. The drug responses are presumably mediated by inducing a change in the activity of membrane bound enzymes. CPZ is very potent in inhibiting the alkaline phosphatase activity in rat brain. The combined effect of CPZ with other drugs shows that CPZ and imipramine together inhibit the enzyme activity significantly greater than the individual inhibition either by CPZ or by imipramine alone. Effective inhibition of the alkaline phosphatase activity with a single drug or combined drugs may lead to a change in neuronal permeability through Trental Pentoxifylline Tablets glucocorticoids thereby affecting mood.

tofranil 25mg tab 2017-03-17

The results of longlasting experience in the treatment of severe chronic pain are reported. 82% of 103 in-patients with chronic pain responded to a combined treatment Aciphex 20 Mg with neuroleptic and antidepressant drugs. A dosing strategy for the combbination of clomipramine and haloperidol is described.

tofranil drug category 2017-01-27

This study was designed Neurontin 300 Mg to compare the efficacy of two two-phase pharmacological treatment strategies for inpatients with DSM-IV major depressive disorder.

tofranil and alcohol 2015-08-16

The present study investigated the effect of monoamine oxidase inhibitors, nialamide which is a non specific monoamine oxidase inhibitor (MAOI), toloxatone which is a A type MAOI and L-deprenyl which is a B type MAOI compared with classical tricyclic antidepressants (clomipramine, desipramine and imipramine), on the escape deficit induced by inescapable shocks (learned helplessness paradigm). Rats were first exposed to inescapable shock pretreatment (60 Symmetrel 100 Mg shocks, 15 sec duration, 0.8 mA, every minute + 15 sec) and 48 h later, shuttle box training (30 trials/day, 15 min.) was initiated in order to evaluate interference effect. Rats with inescapable shocks exhibited escape and avoidance deficits when tested for subsequent responding in a shuttle-box. Daily i.p. injections of nialamide (8 and 16 mg/kg), toloxatone (16 and 32 mg/kg), L-deprenyl (32 and 64 mg/kg) and tricyclic antidepressants (clomipramine: 16 and 32 mg/kg, desipramine: 16 and 24 mg/kg, imipramine: 16 and 32 mg/kg) eliminated escape deficits. In rat exposed to inescapable shocks and treated with L-deprenyl (16 mg/kg/day), nialamide (32 mg/kg/day) or toloxatone (64 mg/kg/day), avoidance responses are significantly increased as compared with non drugged rats preexposed to inescapable shocks. These data extend previous results bearing on the similarity of action of MAOI and tricyclic antidepressants in learned helplessness paradigm (Sherman et al., 1982) and are in agreement with data obtained in other animal models of depression.