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Tofranil (Imipramine)
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Tofranil

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.

Description

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.

Dosage

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.

Overdose

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.

Storage

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.

Contraindications

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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We report a patient in whom cyproheptadine-induced hepatitis was followed by prolonged cholestasis marked by elevation of serum alkaline phosphatase levels, gammaglutamyltransferase and bile acid levels, and disappearance of small bile ducts. Chlorpromazine and imipramine, which can induce a similar acute hepatitis followed by protracted cholestasis, have a close chemical structure (i.e., a tricyclic ring). We suggest that this structure might be involved in this type of hepatotoxicity.

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Autism is a neurodevelopmental disorder, with a multifactorial etiology, characterized by severe abnormalities in communications, social awareness and skills, and the presence of restrictive and stereotyped patterns of behaviors. It is traditionally considered a "static" encephalopathic disorder without any specific cure and few effective biomedical interventions. There are various factors which are involved in the etiopathogenesis of autism or autism spectrum disorder (ASD) such as impaired immune responses, neuroinflammation, abnormal neurotransmission, oxidative stress, mitochondrial dysfunction, environmental toxins and stressors. The autism is often associated with a number of genetic disorders such as fragile X syndrome, tuberous sclerosis, epilepsy and Down syndrome. The recent approaches to autism treatment included various non-pharmacological and pharmacological therapy such as food supplementation, detoxification, treatment of neuroinflammation, immunologic treatments and psychotropic medications, which are found to be effective in treating various behavioral symptoms of autism. In current practice, there is no curative treatment for autism but the recommended treatment for autism involves educational therapies: speech therapy, sensory integration therapy, auditory therapy. There are classes of different pharmacological agents which are found to be effective in improving behavioral symptoms of ASD such as neurotransmitter reuptake inhibitors (fluoxetine), tricyclic antidepressants (imipramine), anticonvulsants (lamotrigine), atypical antipsychotics (clozapine), acetylcholinesterase inhibitors (rivastigmine), etc. New classes of drugs with novel mechanisms of action should be there so that this disorder will become less prevalent in the future.

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There are at least two theoretical reasons to believe antidepressants might help in smoking cessation. Nicotine withdrawal may produce depressive symptoms or precipitate a major depressive episode and antidepressants may relieve these. Nicotine may have antidepressant effects that maintain smoking, and antidepressants may substitute for this effect. Alternatively, some antidepressants may have a specific effect on neural pathways underlying nicotine addiction, independent of their antidepressant effects.

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The results showed that moclobemide and imipramine are equally effective in reducing psychic and somatic anxiety in depressed patients, independent of the severity of anxiety or how it was defined. The criterion of 50% decrease of anxiety scores (at week 4) was consistently reached by 60-70% of patients in all drug sub-groups. The time course of effects on anxiety symptoms was similar with both drugs. It ran parallel to the regression of depression, with significant improvement of anxiety symptoms by week 2 on all measures. The frequency of benzodiazepine (BDZ) co-administration was not systematically correlated with the severity of anxiety. Moreover, co-prescription of BDZ did not change the outcome of drug treatment, with respect either to anxiety symptoms or global therapeutic efficacy. In placebo groups, significant negative interactions were found between severity of anxiety and the efficacy of treatment, which decreased with increased anxiety. The incidence of adverse events with moclobemide was barely higher than in the placebo group. Insomnia (4.9%) was the only adverse event significantly higher with moclobemide than with other treatments. Drop-out rates in drug groups were similar (27%) and unrelated to the severity of anxiety. In the placebo group, drop-outs were significantly higher than in drug groups (39%), and were positively correlated with the severity of anxiety.

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The charts of 150 inpatients and 51 outpatients treated with a monoamine oxidase inhibitor (MAOI)-tricyclic antidepressant combination were reviewed. The incidence and severity of side effects among the patients on the combined regimen were essentially the same as those seen in the control groups. There were no deaths or strokes resulting from use of this regimen. The most frequent troublesome side effect was orthostatic hypotension. We conclude that the use of a MAOI-tricyclic combination in oral therapeutic doses is safe. However, the efficacy of this combination has not yet been proved, and it may be particularly toxic if taken in an overdose.

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The take up time of a standardized alimentary material is a simple component of hamster hoarding behaviour. This value was modified by administrations of the following compounds: diazepam, chlorpromazine, meprobamate, apomorphine, d-amphetamine, piribedil, fenfluramine, sulpiride, imipramine, phenobarbital, clonidine and morphine. The change consisted of a varying increase in the take up time, dependent upon the substance and dosage. High doses of chlorpromazine, apomorphine and fenfluramine inhibited the take up. A behavioural study connected with alimentary take up was included in the experiment. Some behavioural modifications (increase or decrease in motor activity, myorelaxation, stereotyped exploration, reciprocating movements) demonstrated differences between the studied compounds related to their pharmacological properties. The immediate consumption of food, without take up and hoarding behaviour, observed with meprobamate treatment, was an interesting and unexpected change in hamster behaviour. The measurement of the take up time and analysis of behavioural modifications may be useful in comparing and preliminary screening of new psychopharmacological compounds.

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Paroxetine is a selective serotonin reuptake inhibitor (SSRI), with antidepressant and anxiolytic activity. In 6- to 24-week well designed trials, oral paroxetine 10 to 50 mg/day was significantly more effective than placebo, at least as effective as tricyclic antidepressants (TCAs) and as effective as other SSRIs and other antidepressants in the treatment of major depressive disorder. Relapse or recurrence over 1 year after the initial response was significantly lower with paroxetine 10 to 50 mg/day than with placebo and similar to that with imipramine 50 to 275 mg/day. The efficacy of paroxetine 10 to 40 mg/day was similar to that of TCAs and fluoxetine 20 to 60 mg/day in 6- to 12-week trials in patients aged > or =60 years with major depression. Paroxetine 10 to 40 mg/day improved depressive symptoms to an extent similar to that of TCAs in patients with comorbid illness, and was more effective than placebo in the treatment of dysthymia and minor depression. Paroxetine 20 to 60 mg/day was more effective than placebo after 8 to 12 weeks' treatment of obsessive-compulsive disorder (OCD), panic disorder, social anxiety disorder (social phobia), generalised anxiety disorder (GAD) and post-traumatic stress disorder (PTSD). Improvement was maintained or relapse was prevented for 24 weeks to 1 year in patients with OCD, panic disorder, social anxiety disorder or GAD. The efficacy of paroxetine was similar to that of other SSRIs in patients with OCD and panic disorder and similar to that of imipramine but greater than that of 2'chlordesmethyldiazepam in patients with GAD. Paroxetine is generally well tolerated in adults, elderly individuals and patients with comorbid illness, with a tolerability profile similar to that of other SSRIs. The most common adverse events with paroxetine were nausea, sexual dysfunction, somnolence, asthenia, headache, constipation, dizziness, sweating, tremor and decreased appetite. In conclusion, paroxetine, in common with other SSRIs, is generally better tolerated than TCAs and is a first-line treatment option for major depressive disorder, dysthymia or minor depression. Like other SSRIs, paroxetine is also an appropriate first-line therapy for OCD, panic disorder, social anxiety disorder, GAD and PTSD. Notably, paroxetine is the only SSRI currently approved for the treatment of social anxiety disorder and GAD, which makes it the only drug of its class indicated for all five anxiety disorders in addition to major depressive disorder. Thus, given the high degree of psychiatric comorbidity of depression and anxiety, paroxetine is an important first-line option for the treatment of major depressive disorder, OCD, panic disorder, social anxiety disorder, GAD and PTSD.

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We subjected Wistar rats to the forced swim test (FST) to compare the effects of two doses of imipramine in physically stressed rats (P: unavoidable electric footshocks), emotionally stressed rats (E: odors), or non-stressed rats (C). Stress or control sessions lasted 35 days. Drug treatments began on day 21 and continued for the next 14 days. E rats were placed for 10 min, once per day for 35 days, in a small non-movement-restricting cage impregnated with urine collected from a P rat. E and P rats exhibited opposite changes in locomotion. After 21 days of stress sessions, P rats displayed the longest immobility times in the FST, followed by E rats. In the P group, on day 7 of treatment (day 28 of the study), imipramine (2.5 mg/kg) reduced immobility time to baseline values. In the E group, immobility time decreased only after 14 days of treatment with the low imipramine dose. The high dose of imipramine (5.0 mg/kg) reduced immobility time at day 7 of treatment in all groups. In conclusion, physical and emotional stress similarly increased immobility time in the FST, but emotional stress appears to be more resistant to imipramine treatment.

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Enuresis is a symptom that is frequently encountered in child psychiatric evaluations. Careful assessment is required to identify specific urologic, developmental, psychosocial, and sleep-related etiologies. For most children with enuresis, however, a specific etiology cannot be determined. Treatment then involves supportive approaches, conditioning with a urine alarm, or medications--imipramine or desmopressin acetate. The psychosocial consequences of the symptom must be recognized and addressed with sensitivity during the evaluation and treatment of enuresis.

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Myotonic dystrophy or Steinert's disease is an autosomal dominant hereditary disease affecting the entire system. Apart from the myotonic phenomenon it involves muscular atrophy, endocrine disorders, baldness, cardiac arrhythmias, hyperglycaemia, cataracts. Over the years a number of drugs have been tried with results on the myotonia that are still debated. They include quinine, corticosteroids, L-DOPA, potassium-binding resins, procainamide, phenytoin, diphenylhydantoin, N-propylajmaline, dantrolene sodium, carbamazepine, imipramine, baclofen, mexiletine. It is emphasised that only the identification of the biochemical defect involved in the disease will permit any efficient treatment of its symptoms or causes.

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Characteristics of hyperactive children, including speculation in regard to etiology, are reviewed. Drug effects studies and drug treatment of hyperactive behavior are examined, and unresolved issues are discussed. Conclusions indicate that individual differences in hyperative children should form the basis for treatment planning, rather than simply treating groups of children under the rubric "hyperactivity."

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The UDP-glucuronosyltransferases (UGTs) comprise a major excretion pathway for diverse endogenous and exogenous substrates. Relations are reported between polymorphisms of exon 1 of UGT1 and drug side effects or carcinogenesis, but few studies exist of common exon polymorphisms that exert influence throughout UGT1 isoforms. We analysed the polymorphism c.1091C>T, resulting in the amino acid substitution of p.P364L, found on common exon 4. We studied 187 healthy, adult Japanese volunteers. The allele frequency was 0.0053. We investigated the effect of p.P364L on glucuronidation of β-estradiol, acetaminophen, propofol, lamotrigine, imipramine and cyproheptadine in an in vitro expression study. The V(max) values for β-estradiol of p.P364L-UGT1A1, 1A3, 1A7, 1A8 and 1A10 were 36.6%, 82.1%, 26.8%, 29.2% and 22.5%, respectively, of the corresponding wild-type. Glucuronidation activity towards acetaminophen of p.P364L-UGT1A1, 1A6, 1A7, 1A8, 1A9 and 1A10 was 50.3%, 46.4%, 17.2%, 44.1%, 5.0% and 42.8%, respectively, of wild-type. Glucuronidation activity towards propofol of p.P364L-UGT1A7, 1A8, 1A9 and 1A10 was 44.0%, 49.8%, 29.0% and 71.1%, respectively, of wild-type. Substrate inhibition was observed in lamotrigine, cyproheptadine and imipramine glucuronidation by wild-type UGT1A4 but vanished for p.P364L. The presence of p.P364L near the UDP-glucuronic acid binding site could lead to extensive reduction of enzyme activity of many UGT1s. Our results suggest that p.P364L is an important mutation that could give rise to adverse effects of various drugs, or carcinogenesis. It is important to study common exon mutations because these can reduce activity of all UGT1 isoforms.

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Neo-natal rats emit ultrasonic vocalizations (USVs) when isolated from their mothers and littermates. Clinically effective anxiolytics reliably reduce USVs, making this behavior a useful animal model of the anxiolytic potential of novel pharmacological approaches to the treatment of anxiety. Here, we assess the hypothesis that USV duration (total time spent vocalizing) is a more sensitive measure of anxiolytic and antidepressant efficacy than USV number by testing established and putative anxiolytics in this model. Negative geotaxis and righting reflex latency were measured to assess sedating properties. The benzodiazepines, CDP (1-10 mg/kg) and diazepam (0.3-3 mg/kg), the 5HT(1A) partial agonist, buspirone (0.3-3 mg/kg), and the mGluR5 antagonist, MTEP (1-30 mg/kg), reduced USV duration at lower doses and to a greater magnitude than USV number. The benzodiazepines, unlike buspirone and MTEP, produced measurable sedation, but it was dissociable from reductions in USV duration. The SSRI antidepressants, fluoxetine (1-30 mg/kg) and citalopram (0.3-30 mg/kg), reduced USV duration more than number with no measurable effect on sedation. The tricyclic antidepressants, imipramine (1-10 mg/kg) and amitriptyline (1-30 mg/kg), had no effect dissociable from sedation. These data support USV duration as a more sensitive and useful measure than USV number in the isolated rat pup model.

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The relative efficacies of various antiarrhythmic drugs in the treatment of ventricular tachyarrhythmias are not well known. This study examined the effectiveness of imipramine, mexiletine, pirmenol, procainamide, propafenone, quinidine, and sotalol in patients with ventricular tachyarrhythmias who were enrolled in the Electrophysiologic Study versus Electrocardiographic Monitoring trial.

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Adipose tissue kinetics of chlorpromazine and imipramine, two drugs which are more lipophilic than thiopental, were studied in the rat. After single i.v. doses, the time-course of drug distribution was followed in adipose and various other tissues, until their concentrations in adipose tissues declined. Under these conditions the two drugs behaved almost identically. Among the tissues analyzed, the lowest concentrations were found in adipose tissue, with the exception of plasma. At its maximum concentration after about 30 minutes, total adipose tissue contained only 3% of the dose of administered drugs. Adipose/plasma and adipose/lung concentration ratios were 2-5 and 0.05, respectively. After maximum tolerated oral doses of imipramine for 3 weeks, similar steady state concentration ratios (plasma:adipose:brain:lung 1:3:12:96) were observed. In adipose tissue the imipramine/desmethylimipramine ratio was about 1, and the desmethylimipramine steady state levels did not increase with time. Literature data indicate that many basic lipophilic drugs are not stored in adipose tissue. This is now clearly shown for chlorpromazine and imipramine, even under extreme, subchronic conditions in the case of imipramine.

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To determine the possible role of endogenous opioid peptides in the action of imipramine and paroxetine in painful diabetic neuropathy, beta-endorphin concentrations in plasma were measured in 20 patients during a double-blind, placebo-controlled randomized three-way crossover trial. Despite a significant reduction in neuropathy symptoms during both imipramine and paroxetine treatment, the beta-endorphin level was unaltered throughout the study. The plasma concentration of beta-endorphin was not related to plasma drug concentrations. Thus, this study does not provide evidence of a role of endogenous opioid peptides in the mechanism of action of imipramine and paroxetine in painful diabetic neuropathy.

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Spontaneously Hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats differ in their emotional responses to stress and antidepressant administration. We have analysed different neurochemical and psychoneuroendocrine responses to repeated pretreatments with fluoxetine, imipramine or desipramine (10 mg/kg p.o. daily for 4 weeks) in SHRs and WKY rats exposed to a daily 2-h restraint episode for the last 5 days of antidepressant administration. Following a 24-h wash-out period, WKY rats displayed higher plasma antidepressant and antidepressant metabolite levels than SHRs. Fluoxetine pretreatment decreased [(3)H]citalopram binding at midbrain serotonin (5-HT) transporters, whereas tricyclic and/or fluoxetine decreased [(3)H]ketanserin binding at cortical 5-HT(2A) receptors, [(3)H]CGP-12177 binding at cortical ss-adrenoceptors, and [(3)H]nisoxetine binding at midbrain noradrenaline (NA) transporters in both strains. None of the antidepressants affected [(3)H]8-hydroxy-2-(di-N-propylamino)tetralin binding at hippocampal 5-HT(1A) receptors. In WKY rats, repeated restraint triggered a desipramine-sensitive 140% increase in hypothalamus [(3)H]nisoxetine binding; moreover, plasma adrenocorticotropin-releasing hormone responses to a 5-min open field test were amplified by prior repeated restraint in both strains, but desipramine prevented such an amplification in WKY rats only. However, neither elevated plus-maze nor open field behaviors of SHRs and WKY rats were affected by desipramine pretreatment. Thus, the SHR and WKY rat strains may prove useful in understanding how genetic differences in noradrenergic responses to repeated stress and desipramine treatment impact on adaptive processes.

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Examination showed blue-gray facial pigmentation. Light microscopy showed perivascular pigment granule deposits in the upper dermis that stained positively with Fontana-Masson stain and negatively with Prussian blue stain. Electron microscopy showed electron-dense bodies within histiocytes without clearly identifiable melanin granules, consistent with drug-induced pigmentation. Six weeks after switching to sertraline the patient reported a slight improvement of her cutaneous pigmentation.

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Clitoral priapism is a rare condition that is associated with an extended duration of clitoral erection due to local engorgement of clitoral tissue resulting in pain. Although the pathophysiology is not completely understood, it has been associated with specific classes of medications, diseases that alter clitoral blood flow or others associated with small to large vessel disease. We present a case report of a 26-year-old patient who developed clitoral priapism without a clear medication or disease related etiology. The patient was treated with opiates, imipramine, non-steroidal anti-inflammatory medication, and local ice packs. She recovered uneventfully.

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The predictive influence of atypical features was not accounted for on the basis of depression severity.

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Results summarize a comprehensive survey of psychotropic effects on messenger ribonucleic acid (mRNA) expression evident in published data for 70 genes linked to PD risk.

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The effect of chronic treatment with antidepressant drugs fluoxetine (20 mg/kg) and imipramine (25 mg/kg) on the number of antibody-producing cells and the main T cell subpopulations in ASC mice characterized by genetic predisposition to depression-like states was studied at the peak of the SE-induced immune response (5×10(8)). Fluoxetine produced an immunostimulatory effect manifested in an increase in the relative and absolute number of IgM antibody-producing cells in the spleen and index of immunoreactivity (CD4/CD8). Administration of fl uoxetine to parental mouse strains without depression (CBA and AKR) had no effect (CBA) or reduced the immune response. The CD4/CD8 ratio did not increase under these conditions. Imipramine was ineffective in the correction of immune reactions in a depression-like state.

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Ro 11-2465, a cyanide derivative of imipramine with serotonin uptake inhibitory properties, was investigated in six healthy volunteers for its effect on serotonin concentration in blood platelets. The initial dose was 1 mg daily, the maximum dose of 3 mg being reached on day 3 and maintained for 7 days. A significant decrease in the platelet serotonin concentration was not observed until 3 days after the start of drug administration, after which depletion was rapid. After 5 days of treatment, the reduction was about 80% compared to pre-drug level. Serotonin restoration after drug withdrawal was very slow, and 5 days after discontinuation, it was still 70% below its baseline level.

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Several authors have associated the cardiotoxicity of the tricyclic antidepressants with their capacity to potentiate the response to catecholamines. Trazodone is a psychotropic drug with a clinically proven antidepressant activity. It differes from the tricyclic antidepressants under several aspects (chemistry, pharmacology, mode and mechanism of action, etc.), including interactions with catecholamines. Contrary to the tricyclic antidepressants, it does not potentiate the response to catecholamines, but, instead, has an adrenolytic activity. We therefore decided to compare the cardiotoxicity of trazodone and of a tricyclic antidepressant, i.e. imipramine in the rat. The experiments were conducted on anaesthetized Long Evans rats, the drugs being administered by i.v. infusion until cardiac arrest occurred; ECG (lead II) and blood pressure (BP) were recorded at the same time. The primary effect of trazodone was its hypotensive action. ECG changes, consisting of a lengthening of the PR interval, were observed only when there was a marked drop in BP. The primary effect of imipramine, instead, consisted of disturbances in cardiac conduction. It is concluded that trazodone and imipramine produce different cardiovascular effects.

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This study was conducted to demonstrate stable performance using the FCN avoidance procedure, and examine the effects of drugs previously shown to affect impulsive behaviour using a conventional FCN schedule.

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With its chronic administration in a dose of 100 mg/kg lithium carbonate inhibited shaking of the head induced in mice with 5-hydroxytryptophan (5-HTP). This effect did not differ from the action following a single injection of lithium, when the interval between injection of lithium and of 5-HTP was one hour. With the interval lengthened to 24 hours the frequency of shaking diminished only under the effect of chronic administration. At the 5th, 10th and 21st day of a daily administration lithium failed to produce any effect on the hypothermal action of a reserpine-like agent Po 4-1284, but would reduce the protective action of imipramine in a ptosis test. A single injection of lithium made against the background of a chronic injection of water produced an opposite effect, viz. it significantly reduced the protective action of imipramine in hypothermia, but did not affect it with reference to ptosis. Hence, chronic administration of lithium leads to potentiation in its action of the serotonin-negative and central adreno-negative componets and to extenuating the peripheral adreno-negative component.

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tofranil drug classification 2015-05-21

Imipramine binding (IB) was studied in the blood platelets from normal controls and depressed patients over a 4-year period (1981-1984) to determine if seasonal variation was present in Bmax or KD. Bimonthly variation in the Bmax of IB was found in normal controls studied longitudinally. No such variation was found when individual values from normal controls were examined on a monthly or seasonal basis. Bmax in depressed patients showed a significant seasonal, but not monthly, variation. KD of buy tofranil IB varied in normal controls using monthly or seasonal data, but not in the probably more reliable bimonthly data. These results suggest that IB studies comparing groups of subjects should match groups for season of the year or, for greater accuracy, month of the year.

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The effect of imipramine, desipramine, ketanserin and lithium on Type II glucocorticoid receptor (GR) mRNA levels was studied in rat brain regions involved in the control of the hypothalamo-pituitary-adrenal (HPA) axis, the dysregulation of which has been implicated in the pathophysiology of major depression. Northern blot analysis of Type II GR mRNA showed that treatment of male rats with either desipramine or imipramine increased hypothalamic and hippocampal GR mRNA levels. Upregulation of GR mRNA following administration of imipramine was found in brain regions of female rats, while desipramine had no effect. Ketanserin increased levels of GR mRNA in hippocampus of male, but not female, rats. Lithium also was able to induce important increases rat brain GR mRNA; this effect was particularly marked in females. We conclude that desipramine, imipramine, ketanserin and lithium can modulate GR mRNA in regions of rat brain involved in the control of the HPA axis and may have a common mechanism of action buy tofranil at the level of the GR gene. Sexual dimorphism for drug regulation of brain GR mRNA content was shown and may be related to sex differences in the prevalence of certain affective disorders.

tofranil reviews anxiety 2015-12-01

A previous report indicated that the tricyclic antidepressants imipramine and amitriptyline markedly increased plasma prolactin levels in man. We found no buy tofranil increases after acute or chronic treatment with either drug in usual clinical doses. The results indicate that blockade of serotonin reuptake does not affect basal prolactin levels in man.

tofranil drug interactions 2016-04-11

The effect of cimetidine and ranitidine on the demethylation of imipramine (IMI) and on buy tofranil the hydroxylation of desmethylimipramine (DMI) was studied in microsomes from four human livers. Cimetidine inhibited both demethylation of IMI and 2-hydroxylation of DMI, whilst the effect of ranitidine was not statistically significant. 2-hydroxylation of DMI is probably mediated by debrisoquine hydroxylase, a cytochrome P-450 isozyme that is monogenically controlled. The results suggest that cimetidine inhibits this enzyme.

tofranil drug information 2015-06-24

The use of escalating doses of oxybutynin in combination with desmopressin achieved an overall response rate of 96.7% defined as a 2-week period without any enuretic events following initiation of treatment. Low-dose combination therapy (LDCT) (0.6 mg of desmopressin+5 mg of oxybutynin) had a response rate of 68% (Table). Advanced dose combination therapy (ADCT) (0.6 mg of buy tofranil desmopressin+7.5-10 mg of oxybutynin) had a response rate of 75.0%. A statistically significant relationship was found correlating both attention deficit disorder/attention-deficit hyperactivity disorder(ADD/ADHD) and CDVS with failure on monotherapy. No patients in the study reported any adverse events or side effects from the medications.

tofranil tablets 2017-03-05

The motor activity and changes in the latent periods of motor responses were studied in 100 patients with circular and involutional depression, following a single administration of 50 mg of melipramine. A certain correlation was found between the degree of impairment of lability of neural processes and the therapeutic activity of antidepressants. The latter's use was more advisable in patients with milder inertia of neural buy tofranil processes. Four prognostic criteria enabling a reliable prognosis of the immediate effect of amitriptyline and melipramine have been ascertained. These include the speed of formation of a motor stereotype, a sufficient rate of motor responses, and reduction of their latent periods following a single administration of 50 mg of melipramine.

tofranil user reviews 2015-12-04

Based on the results of an open trial with Ro 8-1998 (chemic name: N,N-dimethyl-3-(1-methyl-5H-dibenzo(a,d)cycloheptene-5-ylidene)-propylamine N-oxide hydrochloride) in 11 endogenous depressed outpatients a double-blind trial with imipramine was proposed. Therapeutic efficacy and side effects of Ro 8-1998 and imipramine were compared in a double-blind trial with 30 patients who were newly hospitalized. Most of them suffered from endogenous depression. On days 0, 5, 10, 15 and 20 the patients were examined and the symptoms were documented buy tofranil with the AMP system, the Hamilton scale for depression, a behaviour rating and the "global depression rating Zurich". Ro 8-1998 caused a decrease of systolic blood pressure, an increase of heart frequency and urea. Twelve out of 15 patients showed a decrease of white blood cells. In four patients the number of white blood cells dropped below 4,000. Statistical analyses proved both substances to be potent antidepressants. The therapeutic efficacy of Ro 8-1998 was at least equal to that of imipramine. Further trials with bigger groups of patients are necessary to show whether the trend towards a better antidepressant efficacy of Ro 8-1998 can be reproduced.

tofranil medication 2017-09-05

The differential display method was used to identify the intrinsic factor that changes its mRNA expression level in rat brain after a 14-day oral administration of 20 mg/kg imipramine. The expression of a 180-bp band was markedly enhanced by imipramine. The results of sequencing and a data base search revealed that the isolated clone was glyceraldehyde-3-phosphate dehydrogenase (GAPDH) with a one-base difference. Enhancement of the expression by imipramine was observed in the amygdala. Quantitative PCR showed that imipramine treatment significantly elevated the GAPDH/beta-actin ratio in the cortex. These findings suggest that buy tofranil long-term treatment with imipramine stimulates GAPDH mRNA expression.

tofranil bedwetting reviews 2015-07-02

Emotional rage and fear were found to destroy the differential inhibition and the short-term memory in cats. Stelazine, haloperidol, amitriptyline, imizine, chlordiazepoxide, diazepan and benactyzine prevented these disturbances. Chlorpromazine, as well as stelazine and haloperidol in high doses, enhanced these buy tofranil disturbances. The tranquillizers and the antidepressants normalized the higher nervous activity at a greater dose range than neuroleptics and were more preferable for the elimination of the negative consequences of the strong emotional reactions.

tofranil online 2015-05-10

A comparative metabolism study was performed for bufuralol, dextromethorphan, imipramine, mianserin, sparteine, tamoxifen, haloperidol and two drug candidates (Rec27/0110 and Rec15/2739) on V79 cells genetically engineered to express human cytochrome P450 (CYP) variants 2D6*1, 2D*2, 2D*9 and 2D*17. Unexpectedly, the CYP2D6*17 dependent metabolism profile of haloperidol and Rec27/0110 were found to differ from all other substrates tested. Some of these known standard substrates are frequently applied in marker reactions for CYP2D6 and with these standard substrates, CYP2D6*1 is known to be the most active form. In both cases of haloperidol and Rec27/0110 the variant form CYP2D6*17 had equal or higher activity compared to the CYP2D6*1 form. Results obtained with the V79 cells were confirmed using microsomal preparation of yeast cells expressing the variants CYP2D6*1 and CYP2D6*17 and CYP2D6 inhibitor quinidine. In conclusion, there is no general rule for a variant dependent metabolism profile by cytochrome buy tofranil P450 2D6 indicating that the activity profile of the CYP2D6 alleles may be substrate specific, thus may be reflected in pharmacokinetics consequences for individuals.

tofranil 300 mg 2016-10-27

Ever since the discovery that the classical antidepressants--tricyclics and MA oxidase inhibitors--exert an influence on central 5-HT, this neurotransmitter has been studied in depression, particularly in those forms responsive to this type of treatment. This chapter reviews the evidence in favor of a relationship between depression and central 5-HT dysfunctions. Most of the findings have been derived from patients with depression as the principal diagnosis. Some data have originated from patients suffering from a somatic illness and from depression as well. Both peripheral and central data are discussed. Although no single 5-HT-related finding in depression has so far been unequivocally established, the available evidence, in balance, justifies the tentative conclusion that disturbances in 5-HT metabolism can occur in depression. Lowered CSF 5-HIAA, the major indicator of disturbed central 5-HT metabolism in depression, has also been reported in aggression disorders, both in patients who had committed suicidal acts and in those with outward-directed aggression. The finding can not be explained by a concomitant buy tofranil state of depression. Rather than to discard the classical 5-HT-depression hypothesis, in favor of a 5-HT-aggression hypothesis, the hypothesis is launched that disturbances in serotonergic regulation can give rise to both mood and aggression disorders. This would provide a biological explanation for the clinical observation that those disorders frequently go hand in hand.

tofranil medicine 2016-09-21

We examined whether the antidepressant drugs, such as the dicyclic drug zimeldine, the tricyclic drug imipramine, tetracyclic drug maprotiline, and the non-cyclic drug nomifensine, inhibit in vitro semicarbazide-sensitive amine oxidase (SSAO) activity in monkey brain. The deamination of 1 microM buy tofranil benzylamine was not inhibited at high concentrations of clorgyline or deprenyl, while it was highly sensitive for semicarbazide. When corresponding experiments were performed with 100 microM benzylamine, the opposite results were obtained. The most potent of inhibition of SSAO was observed by imipramine, followed by maprotiline, zimeldine and nomifensine. Inhibition of SSAO was not enhanced by varying the time of preincubation of the enzyme and various antidepressant drugs, indicating direct action on and reversible inhibition of SSAO. We found the tricyclic antidepressant drug to be the most selective inhibitors of SSAO activity in monkey brain, as compared with other type of antidepressant drugs.

tofranil 10 mg 2016-03-09

The taste of six psychotropic drugs (amitriptyline HCl, clomipramine HCl, desipramine HCl, imipramine HCl, doxepin HCl, and trifluoperazine HCl) can be detected at concentrations of 0.1 mM or less in both young and elderly individuals. At concentrations 4 times higher than the detection thresholds, these drugs have bitter buy tofranil as well as other unpleasant taste properties. Oral exposure to these drugs not only induces a taste from the drug itself but also alters taste perception of other compounds such as NaCl and sucrose. These results indicate that both hypogeusia and dysgeusia may be induced by psychotropic medications.

tofranil maximum dosage 2015-07-03

Most of the pre-clinical tests used to assay the efficacy of prospective new agents are done with male experimental animals. In this case, a large part of the population is disregarded as is the interaction of the new agent's effects with female hormonal fluctuations. The present study reviews the technical procedures characteristic for the forced-swimming test and the behavioral outcome induced by the testing procedure in males. It also compares the anti-immobility effects of the classic antidepressant imipramine (IMI) in male and female rats using a detailed behavioral scoring. Female rats had vaginal smears done before the beginning of the behavioral testing and were administered with three doses 24 h, 5 h and 1 h before the retest, as were male rats. Tests were videotape-recorded for analysis of the frequency and duration of the behaviors during forced-swimming. Male rats spend around 50% of the time immobile during the retest. There was a significant, dose-dependent decrease in immobility duration and a decrease in head-shakes of male rats treated with IMI. Both active behaviors of climbing and swimming were equally enhanced by the tricyclic antidepressant, climbing behavior comprising 75% of the mobile behaviors. Females showed much lower immobility duration and head-shake frequency during the forced-swimming than males and spent longer periods in mobile behaviors. Imipramine only decreases immobility frequency and head-shakes of females, and increases buy tofranil the escape-type behavior of climbing, decreasing swimming in the middle of the tank. This effect is more noticeable during estrus and proestrus. These results demonstrate the main behavioral differences between males and females in the forced-swimming test. It also elucidates that the effects of imipramine are measurable in males using the duration of the behaviors, while the frequencies of behaviors are modified in females treated with imipramine.

tofranil drug class 2016-10-26

The aim of the study was to determine the long-term efficacy of the tricyclic antidepressant (TCA) drugs amitriptyline or imipramine in treating functional gastrointestinal disorders (FGIDs Rulide With Alcohol ) in pediatric patients.

tofranil brand name 2017-12-15

It is found, that aggression which occures in rats under inevitable painful stimulation is coursed as excessive excitation of the rats. This aggression may be used for revealing the sedative effect of drugs. The method of fighting for the stool which is caused by motivated fighting for the territory was worked out. This motivated aggression may be used for revealing the tranquillizing effect of drugs. Using these methods it is found Atarax Dosing that stelasine, haloperidol, amitriptyline, imipramine, chlordiazepoxide, diazepam and benactyzine in small doses have a tranquillizing effect, while pentobarbital and chlorpromazine have primarily a sedative effect.

tofranil dosage 2015-04-07

Amiodarone is a clinically effective antiarrhythmic drug shown to cause lung damage in humans and animals. While the mechanism of this pulmonary toxicity is unknown, it may be associated with the accumulation of amiodarone and Omnicef Pediatric Dosage its principal metabolite, desethylamiodarone, by alveolar macrophages. In the present study, characteristics of the uptake of these drugs by rat alveolar macrophages in vitro were examined. The alveolar macrophages were collected by pulmonary lavage from male Fischer 344 rats. Amiodarone and desethylamiodarone were incubated separately (2.5 microM) with the cells in culture for 1, 2, 4 and 18 hr. High performance liquid chromatography was used to measure drug uptake. At 1 and 2 hr, the uptake of desethylamiodarone by alveolar macrophages was significantly greater (P less than 0.05) than that of amiodarone, but over time, the accumulation of amiodarone began to approach that of desethylamiodarone and was not significantly different by 4 hr. To simulate a more physiological situation, plasma levels achieved in the adult male rat after 1 week of amiodarone treatment (150 mg/kg) were used. Amiodarone (1.95 micrograms/mL) and desethylamiodarone (0.80 microgram/mL) were added together into the cell culture. At 1 and 18 hr, the ratio of desethylamiodarone/amiodarone uptake was significantly greater (P less than 0.05) than in incubation medium containing no cells, indicating an enhanced uptake of desethylamiodarone. Metabolic inhibitors (KCN, 2,4-dinitrophenol, and ouabain) and other cationic, amphiphilic drugs (chlorcyclizine, chlorphentermine, and imipramine) were added individually to the cell cultures containing amiodarone or desethylamiodarone. During 1 hr of incubation, these agents had no effect in blocking the accumulation of amiodarone and desethylamiodarone in the cells. The efflux of amiodarone or desethylamiodarone was measured from cells following incubation for 4 hr with each drug. After this time, the medium was replaced with drug-free medium, and the cells were incubated for another 24 hr. Sixty-three percent of amiodarone was lost as compared to only 31% of desethylamiodarone over the 24-hr period (P less than 0.05). The results of this study are suggestive of a preferential uptake and retention of desethylamiodarone as compared to amiodarone. The accumulation of the drugs appears not to be due to active transport or associated with any carrier protein involved in the transport of other structurally-related compounds.

tofranil tabs 2016-08-07

In the rat hypothalamus [3H]imipramine binding is inhibited by tricyclic and nontricyclic antidepressant drugs in a complex manner, with biphasic curves and Hill coefficients less than 1.0. 5-Hydroxytryptamine (serotonin) inhibited with high affinity a decreasing proportion of the [3H]imipramine Diovan Maximum Dosage binding sites as the [3H]imipramine concentration was raised. In the absence of sodium ions, IC50 values for the inhibition by tricyclic and nontricyclic antidepressants were increased by approximately 1,000-fold, and the inhibition curves became classically monophasic with Hill coefficients close to 1.0. These data are interpreted as suggesting that [3H]imipramine binds to two independent sites in the rat hypothalamus. One site is sodium-dependent with a high affinity for the drugs tested; the other is sodium-independent and has a low affinity for these drugs.

tofranil 35 mg 2017-07-25

The effects of ladasten and reference product imipramine (10 mg/kg) on the content of cytokines TNF-α, IL-6, IL-10, IL-1α, IL-2, IL-4, IL-5, IL-17, IFN-γ, and GM-CSF and behavior of male C57Bl/6 mice were studied on the model of a depression-like state induced by a single intraperitoneal injection of bacterial LPS in a dose of 100 μg/kg. Ladasten was injected 5 times in doses of 30 and Duricef Oral Suspension 50 mg/kg. LPS was administered 1 h after the last injection of the test agents. Behavioral disturbances and significant increase in the concentration of TNF-α and IL-6 in blood plasma were observed 2 h after LPS treatment. Ladasten was more potent than imipramine in decreasing the content of proinflammatory cytokines TNF-α and IL-6 and preventing the development of behavioral disturbances in mice. Antiasthenic drug ladasten was shown to decrease the elevated level of proinflammatory cytokines TNF-α and IL-6 after LPS treatment. Further studies should be performed to develop new indications for the use of ladasten in adjuvant therapy of depression.

tofranil street drug 2016-02-16

After discussing potential alternative interpretations of the drug-induced changes of EFs Paracetamol Dosage , we propose the DH test as a useful test for assessing a drug-induced, depressive-like state that may contribute to neuroleptic dysphoria.

tofranil pm reviews 2016-12-13

The Dominant-Submissive Relationship (DSR) model used here was developed for mood stabilizing and antidepressant drug testing. Treatment of submissive Flomax Online animals with known antidepressants significantly reduced submissive behavior in a dose-dependent manner. We hypothesized that if submissive behavior in DSR is a valid model of depression, it should be possible to show a genetic predisposition for this trait, since clinical studies support a genetic component for depression.

tofranil generic name 2015-04-02

1. The role of putative neurotransmitters was investigated in morphine-induced Straub reaction (SR) in albino mice. 2. Apomorphine (15 mg/kg) was also effective in inducing SR. However, in a smaller dose (0.2 mg/kg) it blocked SR induced by morphine. 3. Morphine-induced SR was potentiated by tranylcypromine, reserpine (acute effect), imipramine and L-dopa and blocked by reserpine ( Cleocin 300 Dosage chronic effect), alpha-methyldopa, pimozide, chlorpromazine, haloperidol and metoclopramide. Prazosin and clonidine partially blocked morphine SR in high doses. 4. Propranolol, yohimbine, cyproheptadine and atropine were ineffective in blocking morphine SR. 5. The results indicate that morphine SR is mediated through release of DA in the CNS which excites central D2 receptors. Activation of central alpha 1-adrenoceptors might also play a minor role.

tofranil diet pill 2017-01-04

Data obtained from human studies in vivo show that the dispositions of the tricyclic antidepressant drugs desmethylimipramine (DMI) and nortriptyline are related to the debrisoquine hydroxylation phenotype. To obtain insight into the enzymic mechanisms behind this, the metabolism of debrisoquine and antidepressant drugs by human liver preparations have been studied. The 2-hydroxylation of DMI in vitro correlates with the 4-hydroxylation of debrisoquine among various livers (rs = 0.90). Debrisoquine inhibits DMI hydroxylation competitively, and DMI inhibits debrisoquine hydroxylation, suggesting that DMI hydroxylation is catalysed by the debrisoquine hydroxylase in human liver. By monitoring the hydroxylation of DMI in various fractions during separation and purification of cytochrome P-450 from human liver microsomes we have purified a cytochrome P-450 which efficiently hydroxylates this drug. The apparently electrophoretically homogeneous enzyme had a molecular weight of 51,500 and hydroxylated DMI and debrisoquine at rates of up to 0.95 and 0.45 nmol/min . nmol P-450, respectively. This is probably the major debrisoquine hydroxylating cytochrome P-450 in man. Nortriptyline 10-hydroxylation correlates strongly (r = 0.96) with debrisoquine hydroxylation in human liver microsomes. Nortriptyline inhibits DMI-hydroxylation competitively, and the drug also inhibits the 4-hydroxylation of debrisoquine. Thus it is probable that nortriptyline is hydroxylated by debrisoquine hydroxylase. Imipramine N-demethylation did not correlate significantly (P greater than 0.1) with debrisoquine hydroxylation among microsomes from nine livers. However, if a liver from a subject, which was a poor metabolizer of debrisoquine in vivo, was included, a correlation was obtained (r = 0.79, P less than 0.01, N = 10). Imipramine demethylation also correlated with DMI-hydroxylation only if the 'poor metabolizer' liver was included (r = 0.75, P less than 0.05, N = 10). Debrisoquine inhibited imipramine demethylation competitively. The data indicate that imipramine can interact with debrisoquine- and DMI-hydroxylase, but it is uncertain if this enzyme plays an important quantitative role in its demethylation. Ethoxyresorufin O-deethylation correlated with DMI hydroxylation (r = 0.80) in human liver preparations, and DMI inhibited the former reaction in what is probably a mixed competitive-non-competitive inhibition. Liver preparations from a subject who was a poor oxidizer of debrisoquine both in vivo and in vitro had unusually low capacity to metabolize ethoxyresorufin. Thus ethoxyresorufin, at least partly, seems to interact with an enzyme that can metabolize DMI in human liver.(ABSTRACT TRUNCATED AT 400 WORDS)

tofranil missed dose 2017-07-16

By exclusion of the insignificant log-transformed variables, multiple regression analysis for In (desipramine/imipramine) showed that only in (mephenytoin S/R) correlated (p = 0.013; r2 = 0.19). For in (2-hydroxydesipramine/2-hydroxyimipramine) we found that in (mephenytoin S/R) and in (4-chlorophenylbiguanide/chloroguanide) correlated (p = 0.001; r2 = 0.41).

tofranil 200 mg 2016-07-07

The electrophoretic mobility of selected acidic and basic test solutes have been determined in non-aqueous media prepared by adding various combinations of ammonium acetate, sodium acetate, methane sulphonic acid and acetic acid to acetonitrile, propylene carbonate, methanol, formamide, N-methylformamide, N,N-dimethylformamide and dimethylsulphoxide, respectively. The apparent pH (pH*) of these non-aqueous media have been measured and it was found that pH* is an important factor for the separations in non-aqueous capillary electrophoresis. However, in some solvents the concentration of sodium acetate has a strong influence on the mobility despite very small changes in pH*. Due to the fact that a change in one parameter influences a number of other parameters it is very difficult to conduct systematic studies in non-aqueous media and to compare the migration of the species at fixed pH* values from one solvent to another. Thus pH* is only of value for comparison when used with a specific solvent or solvent mixture. The viscosity of the above-mentioned solvents were measured at various temperatures and means to adjust the viscosity of the non-aqueous media used for capillary electrophoresis are discussed and the separation of ibuprofen and its major metabolites in urine is used as an example.

tofranil 75 mg 2016-08-07

Plasma membrane vesicles were prepared from porcine pulmonary artery endothelial cells by a dextran-polyethylene glycol two-phase system. Specific carrier-mediated transport of 5-hydroxytryptamine (5-HT) into the vesicles was examined. Transport required a Na+ gradient (out greater than in) across the membrane, and accumulated 5-HT rapidly effluxed out of the vesicles when the ionophore gramicidin was added. Transport was inhibited by the antidepressant imipramine. 5-HT transport into plasma membrane vesicles appeared saturable and exhibited Michaelis-Menten kinetics (Km 7.4 microM, maximal velocity 217 pmol.min-1.mg membrane protein-1). A 24-h exposure to 95% O2 at 1 atmosphere absolute resulted in a 21% decrease (P less than 0.05) in specific 5-HT transport by plasma membrane vesicles. Hyperoxia also caused a significant (P less than 0.01) decrease in plasma membrane fluidity, as measured with the fluorescence probe 1,6-diphenyl-1,3,5-hexatriene. These results indicate that pulmonary artery endothelial cell plasma membrane vesicles provide a good model for studying 5-HT transport activity in vitro. Hyperoxia affects plasma membrane fluidity and 5-HT transport in pulmonary artery endothelial cells, suggesting a possible cause-and-effect relationship between the two.

tofranil 25 mg 2015-09-08

The effects of tricyclic antidepressants, desipramine and imipramine, and phenothiazines, chlorpromazine and trifluoperazine, on chloroquine (CQ)-resistant and CQ-sensitive lines of P. chabaudi were examined in vivo. In mice that received daily injections of these drugs the growth of CQ-resistant and CQ-sensitive parasites was unaffected or affected very slightly, if at all. A combination of CQ and each drug suppressed the growth of CQ-resistant parasites in a dose-dependent manner. In addition, in CQ-sensitive parasites each drug also increased the susceptibility to CQ. Measurements of CQ levels by high-performance liquid chromatography showed that CQ accumulated in sensitive parasites to more than twice the level in resistant parasites at 2 to 4 hr after an injection of CQ. Verapamil and desipramine substantially increased CQ levels in both CQ-resistant and CQ-sensitive parasites. These results suggest that not only Ca2+ antagonists but tricyclic antidepressants reverse CQ resistance in CQ-resistant parasites and enhance the inhibitory effect in sensitive parasites by increasing CQ levels in those parasites. The effects of Ca2+ antagonists, tricyclic antidepressants, and phenothiazines on a pyrimethamine-resistant line of P. chabaudi were also studied. None of the Ca2+ antagonists (verapamil, nicardipine, and diltiazem) affected the growth of the parasite in combination with 20 mg/kg pyrimethamine. Tricyclic antidepressants and phenothiazines suppressed pyrimethamine-resistant parasites to some extent. However, the extent of this suppression was less pronounced as compared with that of suppression of CQ resistance by the same drugs.

tofranil medication information 2015-02-12

A subset of the obese population (25-30%) has been reported to engage in binge eating at least twice weekly (bingers) and to exhibit personality traits and food attitudes similar to those of normoweight bulimic women (bulimics). Tricyclic antidepressants and opiate antagonists effectively suppress binge eating in normoweight bulimics. This 8-wk placebo-controlled, double-blind trial investigated the effect of naltrexone and imipramine on 33 obese bingers and 22 bulimics. Naltrexone (100-150 mg/d) produced a significant reduction in binge duration in bulimics (36 +/- 16%, median +/- SIQR; P = 0.02) whereas imipramine significantly reduced binge duration in obese bingers (88 +/- 31%; P = 0.02). A strong placebo effect was observed in obese bingers and, although a reduction in binge frequency occurred with both naltrexone and imipramine, it was not significantly different from the effect in placebo control subjects. We conclude that naltrexone and imipramine may be useful agents in the treatment of binge eating.

tofranil syrup 2016-01-29

In order to evaluate the enzymes CPK and LDH as potential biochemical markers of tricyclic antidepressant (TCA) cardiotoxicity, we prospectively followed 29 patients with TCA overdose. Serum CPK and LDH were obtained on all patients at admission. Population characteristics included a mean age of 33 y, a mean peak serum TCA concentration of 1190 ng/ml and mean maximal QRS interval of 0.10 sec. Seven patients (23%) had admission hypotension, 7 (23%) had severe respiratory depression, 6 (20%) had seizures and 4 (13%) had cardiac arrhythmias. One patient died. Mean admission CPK was 301 IU/L (nl less than 230 IU/L) while mean LDH was 221 IU/L (nl less than 250 IU/L). In 17 patients (57%), CPK remained in the normal range. There was no correlation between blood pressure, maximal QRS interval, serum TCA concentration, arrhythmias or seizures and CPK or LDH by regression analysis. CPK isoenzymes were obtained in 6 patients (both with and without severe myocardial dysfunction). One patient had an MB fraction of 10%; the remaining 5 had no measurable enzymes of myocardial origin. We conclude that modest elevations in CPK or LDH may occur after TCA overdose. These enzymes do not appear to originate from the myocardium and are of no utility in the assessment of antidepressant cardiotoxicity or prediction of clinical course.