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PubMed1984

Electrophysiological and haemodynamic changes with trazodone, amitriptyline and placebo in depressed out-patients.

Fourteen out-patients with major depressive disorder completed a double-blind, randomized, parallel group study using trazodone (n = 6), amitriptyline (n = 5) and matching placebo (n = 3). The average daily doses used were 223 mg and 95.3 mg for trazodone and amitriptyline, respectively, over the 28-day treatment period. Cardiovascular function was monitored with high speed ECG and by determining systolic time intervals. No significant effects of either drug on supine or standing blood pressure were demonstrated. Trazodone increased QTc on Day 1 only, and reduced heart rate and increased the PR interval on Day 15; these effects had disappeared by Day 29. Amitriptyline markedly increased heart rate, PR interval and QTc, and reduced T wave amplitude on Days 15 and 29. Trazodone had no consistent effect on systolic time intervals except to increase the LVET index, whereas amitriptyline increased both PEP index and PEP/LVET ratio on Days 15 and 29. It is concluded that amitriptyline had a much more marked effect on cardiac function than did trazodone.

Adult↗
PubMed2000

Different effects of amitriptyline and imipramine on the pharmacokinetics and metabolism of perazine in rats.

The aim of this study was to search for possible effects of imipramine and amitriptyline on the pharmacokinetics and metabolism of perazine at steady state in rats. Perazine (10 mg kg(-1), i.p.) was administered to rats twice daily for two weeks, alone or jointly with imipramine or amitriptyline (10 mg kg(-1) i.p.). Concentrations of perazine and its two main metabolites (5-sulphoxide and N-desmethylperazine) in the plasma and brain were measured at 30 min (Cmax), 6h and 12h (slow disposition phase) after the last dose of the drugs. Liver microsomes were prepared 24 h after withdrawal of the drugs. Amitriptyline increased the plasma and brain concentrations of perazine (up to 300% of the control) and N-desmethylperazine, while not affecting those of 5-sulphoxide. Imipramine only tended to increase the neuroleptic concentration in the plasma and brain. Studies with control liver microsomes showed that amitriptyline and imipramine added to the incubation mixture in-vitro, competitively inhibited N-demethylation (Ki (inhibition constant) = 16 microM and 164 microM, respectively) and 5-sulphoxidation (Ki = 57 microM and 86 microM, respectively) of perazine, amitriptyline being a more potent inhibitor of perazine metabolism, especially with respect to N-demethylation. Studies with microsomes of rats treated chronically with perazine or tricyclic antidepressants, or both, did not show significant differences in the rate of perazine metabolism between perazine- and perazine+antidepressant-treated rats. The data obtained were compared with the results of analogous experiments with promazine and thioridazine. It was concluded that elevations of perazine concentration were caused by direct inhibition of the neuroleptic metabolism by the antidepressants. Similar interactions, possibly leading to exacerbation of the pharmacological action of perazine, may be expected in man. Since the interactions between phenothiazines and tricyclic antidepressants may proceed in two directions, reduced doses of both the neuroleptic and the antidepressant are recommended when the drugs are administered jointly.

Amitriptyline↗
PubMed2000

Antinociception induced by amitriptyline and imipramine is mediated by alpha2A-adrenoceptors.

The involvement of alpha2-adrenoceptors in the antinociception induced by the tricyclic antidepressants amitriptyline and imipramine was investigated in mice by using the hot-plate and abdominal constriction tests. The antinociception produced by amitriptyline (15 mg/kg, i.p.) and imipramine (15 mg/kg, i.p.) was prevented by reserpine (2 mg/kg, i.p.) and yohimbine (3-10 mg/kg, i.p.) but not by naloxone (1 mg/kg, i.p.), atropine (5 mg/kg, i.p.), CGP 35348 (100 mg/kg, i.p.) and prazosin (1 mg/kg, i.p.). On the basis of the above data, it can be postulated that amitriptyline and imipramine exerted their antinociceptive effect by activation of alpha2-adrenoceptors. Administration of the alpha2A-adrenoceptor antagonist BRL 44408 (1 mg/kg, i.p.) prevented amitriptyline and imipramine antinociception, whereas the alpha2B/C-adrenoceptor antagonist ARC 239 (10 mg/kg, i.p.) was ineffective. These data indicate that the enhancement of the pain threshold produced by amitriptyline and imipramine is mediated by activation of alpha2A-adrenoceptors. Neither tricyclic antidepressants nor the antagonists used impaired mouse performance evaluated by the rota-rod and hole-board tests.

Amitriptyline↗
PubMed1997

Effective prophylactic therapy for cyclic vomiting syndrome in children using amitriptyline or cyproheptadine.

OBJECTIVE: To evaluate our experience using the antimigraine prophylactic drugs, amitriptyline and cyproheptadine, for the prophylactic management of cyclic vomiting syndrome (CVS) in children. METHODS AND PATIENTS: Twenty-seven patients (16 males) ranging in age from 2 to 16 years at diagnosis, fulfilling the diagnostic criteria for CVS and treated prophylactically with either amitriptyline (22) or/and cyproheptadine (6) were identified through retrospective chart review. Individual patient data were corroborated by the attending physician and/or interviews with patients and families. Minimum follow-up time before entry into the study group was 5 months. Patients were stratified according to three treatment outcomes: 1) complete response-no attacks, 2) partial response-50% or greater reduction in frequency of attacks, and 3) no response-less than 50% decrease in frequency of attacks. RESULTS: Of the 22 patients treated with amitriptyline, 16 (73%) had a complete response while 4 (18%) had a partial response. Of the 6 patients treated with cyproheptadine, 4 (66%) had a complete response and 1 (17%) had a partial response. Thus, 91% of the amitriptyline group and 83% of the cyproheptadine group had at least a partial response to therapy. No patients experienced significant side effects to either medication. CONCLUSION: The antimigraine prophylactic drugs, amitriptyline and cyproheptadine, represent effective prophylactic agents for the management of CVS in the vast majority of patients fulfilling the diagnostic criteria for this syndrome.

Adolescent↗
PubMedDate not supplied

Systemic absorption of amitriptyline and buspirone after oral and transdermal administration to healthy cats.

A prospective study was performed to determine the relative availability of buspirone and amitriptyline after oral and transdermal routes of administration in 6 adult cats. For topical administration, drugs were compounded in a transdermal organogel containing pluronic and lecithin (PLO). Using a crossover design, each cat received a single dose of amitriptyline (5 mg) and buspirone (2.5 mg) by the transdermal and oral route of administration with at least a 2-week washout interval between drug treatments. Blood samples were obtained at 0, 0.5, 1, 2, 4, 6, 8, 10, and 12 hours after drug administration for determination of plasma drug concentrations. Plasma concentrations of immunoreactive amitriptyline and buspirone were determined using commercial enzyme-linked immunosorbent assay (ELISA) tests. Systemic absorption of amitriptyline and buspirone administered by the transdermal route was poor compared with the oral route of administration. Until supporting pharmacokinetic data are available, veterinarians and cat owners should not rely on the transdermal route of administration for treating cats with amitriptyline or buspirone.

Administration, Cutaneous↗
PubMed1988

Clonidine interaction in amitriptyline poisoning.

The effect of clonidine on amitriptyline-induced cardiotoxicity was investigated in an experimental rat mode. A continuous infusion of amitriptyline (30 mg/kg/h) was given until the animal died, usually within 2 hours. Fifteen minutes after starting the amitriptyline infusion, 50 micrograms/kg of clonidine was given intravenously over five minutes. This led to an increase in blood pressure and left ventricular end-diastolic pressure. There was no significant change in cardiac contractility. Heart rate decreased. These changes can be explained by an increase in afterload due to peripheral vasoconstriction. No signs of reduced sympathetic outflow were seen on the ECG. The peripheral effects of clonidine dominated over the central effects, which may be due to a competitive inhibition of amitriptyline at central noradrenergic sites. An increased afterload pushes the heart towards failure and increases mortality. In this model, clonidine did not reverse amitriptyline-induced cardiovascular toxicity. It may even be potentially harmful if used to treat tricyclic antidepressant poisoning.

Amitriptyline↗
PubMed1976

[Polygraphic sleep recordings in patients with endogenous depression before and after treatment with amitriptyline-N-oxide (author's transl)].

15 endogenous-depressive patients were treated with 3 X 20 mg amitriptyline-N-oxide for 20 days. Polygraphic sleep recordings were taken during the first seven and last six nights. In a single-blind study the patients were given placebo for the first four days, amitriptyline-N-oxide was applied during the following 13 days and on the last three days placebo was given again. The statistical evaluation showed the following results: a) Latency times up to the first deep sleep and to the first REM-phase decreased under the effect of the substance. b) Relative sleep duration (without wakefulness) increased. c) Actual sleep duration (without wakefulness and stage A) was similar. d) The frequency of awakenings during the night diminished under amitriptyline-N-oxide and increased somewhat when placebo was given again. The original values were not reached. The frequency of awakenings from REM-phases increased during the first three nights of medication and decreased in the last three nights the substance was administered. When placebo was given again, the original values were exceeded. e) Duration of wakefulness after waking up during the night decreased under amitriptyline-N-oxide and increased when the medication was discontinued. Here again the original values were not reached. After waking up during the night most waking time was spent in stage C. A placebo effect can be excluded. The effects of amitriptyline-N-oxide are compared to those of hypnotics, other antidepressants, antipsychotics and tranquilizers in the discussion.

Adult↗
PubMedDate not supplied

Open comparative randomised study of moclobemide versus amitriptyline in major depressive illness (DSM IIIR) in Nigeria.

In a multi-centre study, 60 patients (20 males and 40 females aged 43 +/- 15 and 37 +/- 15 years respectively) with a DSM-IIIR diagnosis of major depressive disorders were randomly assigned to treatment with either Moclobemide (maximum dose 600 mg per day) or Amitriptyline (maximum dose 150 mg per day) for eight weeks. Patients were evaluated pretreatment and over the 8 weeks treatment period using Hamilton Depression Rating Scale (HDRS) and the clinical global impressions (CGI). The Adverse Drug Effects Schedule, clinical, haematological and biochemical status were also evaluated pre, during and post treatment. Of the 60 patients enrolled for the study 54 were found evaluable for efficacy whilst all 60 were evaluated for safety (Adverse Event). On the HDRS and CGI scale there was no significant difference in the therapeutic outcome between the two treatment groups. In the overall clinical assessment rating at the end of treatment 94.1% of patients in the Moclobemide group were rated 'very good to good' and 94.4% with Amitriptyline. Moclobemide appeared to have a slightly better safety profile, the incidence of adverse event was 9.0% compared to 19.0% with Amitriptyline. The drop out rate was 16.7% and 26.7% for moclobemide and amitriptyline respectively. These differences were however not statistically significant. It was therefore concluded that moclobemide is an effective and safe alternative to amitriptyline, with attractive potential for out patients management of depressive illness.

Adult↗
PubMed2000

Paroxetine versus amitriptyline for treatment of depression associated with rheumatoid arthritis: a randomized, double blind, parallel group study.

OBJECTIVE: To compare the efficacy and tolerability of paroxetine (a selective serotonin reuptake inhibitor) with that of amitriptyline (a tricyclic antidepressant) in the treatment of depression in 191 patients with rheumatoid arthritis (RA). METHODS: A randomized, double blind, double dummy, parallel group study. A placebo washout period of 3-7 days was followed by an 8 week active treatment phase during which patients received either paroxetine (20-40 mg daily) or amitriptyline (75-150 mg daily). The primary efficacy variable was the change from baseline in Montgomery Asberg Depression Rating Scale score at endpoint. RESULTS: Paroxetine was as effective as amitriptyline for the treatment of depression, with similar improvements in RA associated pain and disability also seen in both groups. However, paroxetine was better tolerated than amitriptyline, with an overall frequency of adverse experiences of 56.4% and 67.7% in the 2 groups, respectively. The frequency of anticholinergic adverse experiences was much lower in the paroxetine treatment group (18.1% vs 43.8% taking amitriptyline) and paroxetine treated patients also experienced fewer severe (16.0% vs 21.9%), serious nonfatal (0% vs 4.2%), and drug related adverse experiences (12.8% vs 29.2%). CONCLUSION: Tolerability is an important consideration in this patient population, which is largely composed of elderly patients who are taking additional medications for RA. Paroxetine shows a number of advantages in the management of depression comorbid with RA.

Adolescent↗
PubMed2002

Chronic treatment with the antidepressant amitriptyline prevents impairments in water maze learning in aging rats.

Increasing evidence links chronically elevated glucocorticoid levels and cognitive impairments in a subpopulation of aged rodents and humans. Antidepressant drugs improve hypothalamic-pituitary-adrenal axis feedback regulation and reduce plasma glucocorticoid levels. Decreasing the cumulative lifetime exposure to glucocorticoid excess by long-term exposure to antidepressants may prevent the emergence of cognitive impairments in aged rats. To test this hypothesis, we treated middle-aged male Lister hooded rats (16 months) with amitriptyline until they were 24 months of age, and their cognitive function was assessed in the water maze. Performance in the spatial learning task declined significantly with aging (p < 0.01), with 33% of aged controls showing poorer (<2.5 SD) probe test performance than young controls. Amitriptyline treatment from midlife preserved water maze performance with aging (p < 0.01 compared with aged controls) and significantly (p < 0.01) reduced the proportion of poor performers (7%). Measures of anxiety-related behaviors in the elevated plus-maze were significantly (p < 0.05) decreased in the aged rats after amitriptyline. Furthermore, evening plasma corticosterone levels were reduced (30% decrease; p < 0.01 compared with aged controls) after 6 months of amitriptyline. These data suggest that long-term treatment with amitriptyline decreases the prevalence of cognitive impairment in aged rats and that this may, in part, be a consequence of reduced plasma corticosterone levels and reduced anxiety.

Administration, Oral↗
PubMed2002

Gabapentin: new indication. In postherpetic neuralgia when amitriptyline fails.

(1) Postherpetic pain is infrequent, but the incidence increases with age. (2) The reference treatment for postherpetic pain is oral amitriptyline or desipramine. (3) Gabapentin, an antiepileptic agent, is the first drug to be granted specific approval in France for the treatment of postherpetic pain. (4) In two placebo-controlled trials, gabapentin at a dose of between 1 800 and 3 600 mg/day halved the intensity of pain in about one in three patients. In comparison, pain improved in about 50% of patients taking amitriptyline in clinical trials. (5) Both gabapentin and amitriptyline provoke sedation, but dizziness and peripheral oedema are more frequent on gabapentin, while atropinic effects predominate with amitriptyline. (6) Daily treatment is 10 times more costly in France. (7) In practice, the standard treatment of postherpetic pain remains oral amitriptyline or desipramine. Gabapentin is an alternative, given its different safety profile.

Acetates↗
PubMed2005

[Low doses of prazosin potantiates the antinociceptive/analgesic effect of amitriptyline].

In this study, we aimed to reveal the interaction between the tricyclic antidepressant amitriptyline and a1-adrenoceptor antagonist prazosin in mice by using an analgesiometric device hot-plate. Amitriptyline (10 mg/kg) has analgesic effect as expected. Neither of the prazosin doses (0.1, 0.2, 0.5, 1 mg/kg) displayed analgesic effect alone. The combination of lower doses of prazosin (0.1, 0.2, 0.5 mg/kg) with amitriptyline (10 mg/kg) potentiated the antinociceptive effect of this drug. However, the relatively higher dose of prazosin (1 mg/kg) did not effect amitriptyline analgesia. Thus we conclude that the antinociceptive effect of amitriptyline is potentiated by low doses of prazosin.

Adrenergic alpha-Antagonists↗
PubMed2005

Amitriptyline and fluoxetine protect PC12 cells from cell death induced by hydrogen peroxide.

OBJECTIVE: To investigate the potential protective effects of amitriptyline and fluoxetine in a catecholamine cell model. METHODS: Cultured rat pheochromocytoma (PC12) cells were pretreated with amitriptyline or fluoxetine for 24 or 48 hours and were then subjected to neurotoxic insult (200 micromol/L hydrogen peroxide). Cell viability was determined by measurement of the reduction product of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). The enzyme activity of superoxide dismutase (SOD) was determined by a commercial SOD assay kit. RESULTS: The decrease in cell viability induced by hydrogen peroxide was attenuated in PC12 cells pretreated with 100 micromol/L amitriptyline for 24 hours or with 50 micromol/L amitriptyline or 50 micromol/L fluoxetine for 48 hours. Pretreatment with either amitriptyline or fluoxetine was associated with increased SOD activity in PC12 cells. Inhibition of SOD activity with diethyldithiocarbamic acid reduced the cytoprotective action of fluoxetine. CONCLUSIONS: These data suggest that the neuroprotective actions of some antidepressants include the upregulation of SOD activity.

Amitriptyline↗
PubMed2005

Recreational amitriptyline abuse.

UNLABELLED: Amitriptyline is a potent anticholinergics, rarely used as a drug of abuse. Two cases of amitriptyline dependency lasting for almost twelve months were described. According to the patients the abuse with amitriptyline guarantee them safety not to be uncovered by parents and doctors who systematically checked their urine with typical narcotic tests. CASE REPORT: Two patients with a history of abuse with amphetamine and clonazepam were admitted to the Clinic because of intoxication with amitriptyline. They denied the suicidal attempt and explained that they used amitriptyline in a dosage of 100 to 200 mg per day as a drug of abuse. On the day of admission one of the patients had increased the dosage up to 600 mg which caused an acute intoxication. CONCLUSION: Antidepressants should be treated as a drugs with possible abuse ability.

Adult↗
PubMed1991

[Plasma and urine kinetics of amitriptyline oxide and its metabolites. Comparison of intravenous infusion and oral administration in volunteers].

The study objective was to obtain detailed information on the plasma and urine kinetics of amitriptylinoxide (CAS 4317-14-0) and its metabolites. For this reason, 60 mg of amitriptylinoxide was administered to 12 subjects, both by intravenous infusion and by oral dosage, in a study performed according to a randomized two-way cross-over design. In plasma, we succeeded in analyzing the metabolites amitriptyline and nortriptyline in addition to the parent substance amitriptyloxide. The tests for the parent substance amitriptylinoxide revealed maximum plasma levels of 721 and 686 ng/ml at 1.96 h (i.v. infusion) and 0.82 h (oral formulation), respectively. Mean values of 2331 (infusion) and 1714 h.ng/ml (oral formulation) were determined for the area under the curve from time 0 to infinity AUC (0-infinity). We also produced a comprehensive evaluation of amitriptyline, however, this was not possible for the metabolite nortriptyline. In urine, we succeeded in a reliable quantification of 4 metabolites, namely cis-OH-amitriptylinoxide, trans-OH-amitriptylinoxide, amitriptyline and OH-nortriptyline, in addition to the parent substance amitriptylinoxide. In individual samples, nortriptyline, cis-OH-amitriptyline and trans-OH-amitriptyline were additionally identified. In the course of the study, there were no reports or observations of any adverse reactions in addition to the side effects known for amitriptylinoxide from literature. There were no clinically relevant differences in tolerability observed between these two preparations.

Administration, Oral↗
PubMed1990

Steady-state plasma levels during antidepressant therapy with amitriptyline and amitriptylinoxide.

Plasma levels of amitriptyline, amitrypylinoxide, and their metabolites were analyzed in a controlled clinical trial with two groups of depressed patients. After administration of both drugs, demethylated and hydroxylated derivatives proved to be the main metabolites, and to a great extent amitriptylinoxide was reduced to amitriptyline. Continuous oral application of 150 mg/os per day of each drug resulted in therapeutically effective concentrations in both groups; however, concentrations were two to three times higher in the group receiving amitriptyline, rather than amitriptylinoxide. Based on the steady-state plasma levels, the total clearance of amitriptyline was calculated with a magnitude of 7 ml/min per kg. A first-order kinetic model was proposed to estimate the steady-state concentrations of consecutive metabolites, employing available kinetic data. Computed levels of nortriptyline after application of amitriptyline and amitriptylinoxide were 61.1 and 20.3 ng/ml, respectively, compared to nortriptyline levels determined with HPLC, which were 70.1 and 26.5 ng/ml, respectively. The model is discussed in relation to its practical use during monitoring of drug therapy with tricylics.

Adult↗
PubMed1990

A drug utilization review of prescribing patterns for trazodone versus amitriptyline.

The second-generation antidepressant trazodone has been thought by some clinicians to exert a less robust antidepressant effect than do tricyclic agents. This impression differs from the findings of numerous published clinical trials. In an effort to determine whether this discrepancy may be due to possible inappropriate dosing or use of trazodone for different patient subtypes, a retrospective chart review of 138 depressed inpatients treated with amitriptyline and of 42 depressed inpatients treated with trazodone was performed to compare their respective prescribing patterns. While these two groups did not differ with regard to most demographic variables, results revealed that patient prescribed trazodone were older (trazodone, mean +/- SD age = 54.5 +/- 8.8 years versus amitriptyline, 43.2 +/- 12.9 years; p less than .001), more often had a recurrent depressive disorder (trazodone = 57.1%, amitriptyline = 39.1%, p less than .06), and more frequently had a history of unresponsiveness to other antidepressants (trazodone = 47.6%, amitriptyline = 11.6%; p less than .001). In addition, initially prescribed daily doses of trazodone were below the recommended starting dose of 150 mg/day (mean +/- SD starting dose = 113.7 +/- 42.1 mg/day), while starting daily doses for amitriptyline (mean +/- SD = 69.8 +/- 20.1 mg/day) were judged to be more adequate relative to the recommended daily dose of 75 mg/day. Final trazodone dosage (mean +/- SD final dose = 217.9 +/- 87.5 mg/day) could be judged to have been far short of optimal levels of 250 to 350 mg/day and of up to 600 mg/day for inpatients and 400 mg/day for outpatient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Mirtazapine vs. amitriptyline vs. placebo in the treatment of major depressive disorder.

Patients (n = 150) were randomized to a 6-week, double-blind study to evaluate the relative efficacy and safety of mirtazapine, amitriptyline, and placebo in the treatment of major depressive disorder symptoms. Average daily modal doses were mirtazapine, 18 mg; amitriptyline, 111 mg; and placebo, 4.6 capsules. Mirtazapine- and amitriptyline-treated patients had statistically significantly greater mean Hamilton Rating Scale for Depression (HAM-D) score reductions (weekly visits 1, 2, 4, and endpoint) compared to placebo. These findings were supported by the Montgomery-Asberg Depression Rating Scale (MADRS); the Zung Self-rating Depression Scale (SDS); and the Clinical Global Impressions (CGI) scales. Somnolence and weight gain were the only adverse clinical experiences (ACEs) reported substantially more often by mirtazapine-treated patients than by those in the placebo group. However, more amitriptyline-treated patients reported decreased visual accommodation, dry mouth, dyspepsia, constipation, tachycardia, hypertension, hypotension, discoordination, dizziness, and tremor than mirtazapine- or placebo-treated patients. Results of this study indicate that mirtazapine is more effective than placebo in the treatment of these patients, and superior to amitriptyline in respect to anticholinergic and cardiovascular effects.

Adult↗